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Archive for the ‘Cardiac Stem Cells’ Category

Stem cell technology could lead to ailing heart mending …

Tsai et al./Stem Cell Reports 2015

Weill Cornell investigators have discovered how to generate large numbers of rare cells in the network that pushes the heart’s chambers to consistently contract. In this image, investigators stained these cells, generated from embryonic stem cells, to reveal cell-specific genes (green and red, indicated by arrows). The blue represents stained cell nuclei.

For the first time, scientists can efficiently generate large numbers of rare cells in the network that pushes the heart’s chambers to consistently contract. The technique, published May 28 in Stem Cell Reports, could be a first step toward using a person’s own cells to repair an irregular heartbeat known as cardiac arrhythmia.

This study, while done using mouse cells, will now allow us to develop human heart cells and test their function in repairing damaged hearts, said the study’s senior author, Dr. Todd Evans, vice chair for research and the Peter I. Pressman Professor in the Department of Surgery at Weill Cornell Medical College.

The human heart beats billions of times during a lifetime, so it’s not surprising that development of irregular heartbeats can lead to a variety of cardiac diseases, Evans says. But treatments for these disorders are costly, and often ineffective.

The government pays more than $3 billion each year for cardiac arrhythmia-related diseases. Despite this enormous expense, the treatments we have available are inadequate, Evans said. For example, artificial pacemakers are often used, but these can fail, and are particularly challenging therapies for children.

One solution is to coax a patient’s own cells to generate the specific kinds of cells in the cardiac conduction system (CCS) that maintain a regular heartbeat.

We can imagine someday using these cells, for example, to create patches that can replace defective conduction fibers. Of course this is still a long way off, as we would need to study how to coax them into integrating properly with the rest of the CCS, Evans said. But previously, we did not even have the capacity to generate the cells, and now we can do so in a manner that is scalable, so that such preclinical research is now feasible.

Evans worked with Dr. Shuibing Chen, an expert in stem cell and chemical biology, and Dr. Su-Yi Tsai, a postdoctoral fellow and the study’s lead investigator. Other key contributors were from the laboratory of Dr. Glenn Fishman, who specializes in cardiac physiology at New York University.

Their first goal was to increase the efficiency of coaxing mouse embryonic stem cells to become CCS cells. They created mouse stem cells that can express a CCS marker gene that can be quantified. This allows them to measure how many embryonic cells morph into CCS cells.

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Stem cell technology could lead to ailing heart mending …

6. Mending a Broken Heart: Stem Cells and Cardiac Repair …

Charles A. Goldthwaite, Jr., Ph.D.

Cardiovascular disease (CVD), which includes hypertension, coronary heart disease (CHD), stroke, and congestive heart failure (CHF), has ranked as the number one cause of death in the United States every year since 1900 except 1918, when the nation struggled with an influenza epidemic.1 In 2002, CVD claimed roughly as many lives as cancer, chronic lower respiratory diseases, accidents, diabetes mellitus, influenza, and pneumonia combined. According to data from the 19992002 National Health and Nutrition Examination Survey (NHANES), CVD caused approximately 1.4 million deaths (38.0 percent of all deaths) in the U.S. in 2002. Nearly 2600 Americans die of CVD each day, roughly one death every 34 seconds. Moreover, within a year of diagnosis, one in five patients with CHF will die. CVD also creates a growing economic burden; the total health care cost of CVD in 2005 was estimated at $393.5 billion dollars.

Given the aging of the U.S. population and the relatively dramatic recent increases in the prevalence of cardiovascular risk factors such as obesity and type 2 diabetes,2,3 CVD will continue to be a significant health concern well into the 21st century. However, improvements in the acute treatment of heart attacks and an increasing arsenal of drugs have facilitated survival. In the U.S. alone, an estimated 7.1 million people have survived a heart attack, while 4.9 million live with CHF.1 These trends suggest an unmet need for therapies to regenerate or repair damaged cardiac tissue.

Ischemic heart failure occurs when cardiac tissue is deprived of oxygen. When the ischemic insult is severe enough to cause the loss of critical amounts of cardiac muscle cells (cardiomyocytes), this loss initiates a cascade of detrimental events, including formation of a non-contractile scar, ventricular wall thinning (see Figure 6.1), an overload of blood flow and pressure, ventricular remodeling (the overstretching of viable cardiac cells to sustain cardiac output), heart failure, and eventual death.4 Restoring damaged heart muscle tissue, through repair or regeneration, therefore represents a fundamental mechanistic strategy to treat heart failure. However, endogenous repair mechanisms, including the proliferation of cardiomyocytes under conditions of severe blood vessel stress or vessel formation and tissue generation via the migration of bone-marrow-derived stem cells to the site of damage, are in themselves insufficient to restore lost heart muscle tissue (myocardium) or cardiac function.5 Current pharmacologic interventions for heart disease, including beta-blockers, diuretics, and angiotensin-converting enzyme (ACE) inhibitors, and surgical treatment options, such as changing the shape of the left ventricle and implanting assistive devices such as pacemakers or defibrillators, do not restore function to damaged tissue. Moreover, while implantation of mechanical ventricular assist devices can provide long-term improvement in heart function, complications such as infection and blood clots remain problematic.6 Although heart transplantation offers a viable option to replace damaged myocardium in selected individuals, organ availability and transplant rejection complications limit the widespread practical use of this approach.

Figure 6.1. Normal vs. Infarcted Heart. The left ventricle has a thick muscular wall, shown in cross-section in A. After a myocardial infarction (heart attack), heart muscle cells in the left ventricle are deprived of oxygen and die (B), eventually causing the ventricular wall to become thinner (C).

2007 Terese Winslow

The difficulty in regenerating damaged myocardial tissue has led researchers to explore the application of embryonic and adult-derived stem cells for cardiac repair. A number of stem cell types, including embryonic stem (ES) cells, cardiac stem cells that naturally reside within the heart, myoblasts (muscle stem cells), adult bone marrow-derived cells, mesenchymal cells (bone marrow-derived cells that give rise to tissues such as muscle, bone, tendons, ligaments, and adipose tissue), endothelial progenitor cells (cells that give rise to the endothelium, the interior lining of blood vessels), and umbilical cord blood cells, have been investigated to varying extents as possible sources for regenerating damaged myocardium. All have been tested in mouse or rat models, and some have been tested in large animal models such as pigs. Preliminary clinical data for many of these cell types have also been gathered in selected patient populations.

However, clinical trials to date using stem cells to repair damaged cardiac tissue vary in terms of the condition being treated, the method of cell delivery, and the primary outcome measured by the study, thus hampering direct comparisons between trials.7 Some patients who have received stem cells for myocardial repair have reduced cardiac blood flow (myocardial ischemia), while others have more pronounced congestive heart failure and still others are recovering from heart attacks. In some cases, the patient’s underlying condition influences the way that the stem cells are delivered to his/her heart (see the section, quot;Methods of Cell Deliveryquot; for details). Even among patients undergoing comparable procedures, the clinical study design can affect the reporting of results. Some studies have focused on safety issues and adverse effects of the transplantation procedures; others have assessed improvements in ventricular function or the delivery of arterial blood. Furthermore, no published trial has directly compared two or more stem cell types, and the transplanted cells may be autologous (i.e., derived from the person on whom they are used) or allogeneic (i.e., originating from another person) in origin. Finally, most of these trials use unlabeled cells, making it difficult for investigators to follow the cells’ course through the body after transplantation (see the section quot;Considerations for Using These Stem Cells in the Clinical Settingquot; at the end of this article for more details).

Despite the relative infancy of this field, initial results from the application of stem cells to restore cardiac function have been promising. This article will review the research supporting each of the aforementioned cell types as potential source materials for myocardial regeneration and will conclude with a discussion of general issues that relate to their clinical application.

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6. Mending a Broken Heart: Stem Cells and Cardiac Repair …

Bone-Derived Stem Cells Repair the Heart After Myocardial …

Rationale: Autologous bone marrowderived or cardiac-derived stem cell therapy for heart disease has demonstrated safety and efficacy in clinical trials, but functional improvements have been limited. Finding the optimal stem cell type best suited for cardiac regeneration is the key toward improving clinical outcomes.

Objective: To determine the mechanism by which novel bone-derived stem cells support the injured heart.

Methods and Results: Cortical bonederived stem cells (CBSCs) and cardiac-derived stem cells were isolated from enhanced green fluorescent protein (EGFP+) transgenic mice and were shown to express c-kit and Sca-1 as well as 8 paracrine factors involved in cardioprotection, angiogenesis, and stem cell function. Wild-type C57BL/6 mice underwent sham operation (n=21) or myocardial infarction with injection of CBSCs (n=67), cardiac-derived stem cells (n=36), or saline (n=60). Cardiac function was monitored using echocardiography. Only 2/8 paracrine factors were detected in EGFP+ CBSCs in vivo (basic fibroblast growth factor and vascular endothelial growth factor), and this expression was associated with increased neovascularization of the infarct border zone. CBSC therapy improved survival, cardiac function, regional strain, attenuated remodeling, and decreased infarct size relative to cardiac-derived stem cells or saline-treated myocardial infarction controls. By 6 weeks, EGFP+ cardiomyocytes, vascular smooth muscle, and endothelial cells could be identified in CBSC-treated, but not in cardiac-derived stem cellstreated, animals. EGFP+ CBSC-derived isolated myocytes were smaller and more frequently mononucleated, but were functionally indistinguishable from EGFP myocytes.

Conclusions: CBSCs improve survival, cardiac function, and attenuate remodeling through the following 2 mechanisms: (1) secretion of proangiogenic factors that stimulate endogenous neovascularization, and (2) differentiation into functional adult myocytes and vascular cells.

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Bone-Derived Stem Cells Repair the Heart After Myocardial …

Heart Disease – Stemaid : Embryonic Stem-cells

Clara’s Story

Clara had a severe heart attack in 2004. Before contacting us she had received adult stem cells from a company in Thailand – a process requiring at least a one week stay.

When she contacted Stemaid, she had just had an echocardiogram showing that her overall left ventricular ejection fraction was estimated to be 30 to 35%. She opted to receive one injection of 5 million Embryonic Stem Cells by Stemaid in November 2010. She arrived at 1pm and was done by 3pm the same day.

We received the following email from her in April 2011: I had an EKO last week and rate is 44%, up from the 33/35% it was before I received Stemaid’s stem cells! . Are the stem cells still available and still as good?

The heart contains a small amount of stem cells, the cardiac stem cells, that are produced when there is a need for production of more heart cells or for an active replacement of damaged ones. These cardiac cells are produced in high quantity for about one week following an infarction, actively repairing the damaged areas of the heart.

However this high production stops after a week and the repair stops as well.

Initial studies showed that by introducing embryonic stem cells, the heart starts to repair again within minutes of their injection. More recent studies showed that the injection of embryonic stem cells actually triggers the production of cardiac stem cells for one week. Another week of active repair is offered each time that one receives embryonic stem cells.

If you have suffered from an infarction, we suggest a minimum of 3 injections of esc over the course of 3 weeks to get significant repair.

Some of the patients who have received Stemaid Embryonic Stem-Cells have agreed to be mentioned on our website so that we may illustrate the benefits of them.

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Heart Disease – Stemaid : Embryonic Stem-cells

Stem cell therapy : When will it help the heart? | The Why …

Stem cells: When will they heal the heart?

Its been 15 years since a University of Wisconsin-Madison researcher isolated embryonic stem cells the do-anything cells that appear in early development. Its been six years since adult human cells were transformed into the related induced pluripotent stem cells.

ENLARGE

Some day, stem cell therapy could restore cells, save hearts, and avoid the need for some heart transplants, such as this one. This heart is ready for its new home.

And yet the early hope to grow spare parts turning stem cells into specialized cells for repairing a failing brain, pancreas or heart, remains mostly promise rather than reality.

Researchers have since found how to transform stem cells into a wide variety of body cells, including heart muscle cells, or cardiomyocytes. But the holy Grail tissue supplementation or replacement remains tantalizingly out of reach.

Last week, Why Files attended a symposium on treating cardiovascular disease with stem cells, at the BioPharmaceutical Technology Center Institute near Madison, Wis. We found the picture unexpectedly complicated: as multiple kinds of stem cells are grown and delivered in a bewildering variety of ways to treat a catalog of conditions.

So far, stem cells have not been approved to treat any heart disease in the United States.

Still, the need remains clear. Disorders of the heart and blood vessels, which deliver oxygen and nutrients to the body, continue to kill. Today, one of every 2.6 Americans will die of some cause related to their heart, writes Columbia University Medical Center.

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Stem cell therapy : When will it help the heart? | The Why …

9. Can Stem Cells Repair a Damaged Heart? [Stem Cell …

Heart attacks and congestive heart failure remain among the Nation’s most prominent health challenges despite many breakthroughs in cardiovascular medicine. In fact, despite successful approaches to prevent or limit cardiovascular disease, the restoration of function to the damaged heart remains a formidable challenge. Recent research is providing early evidence that adult and embryonic stem cells may be able to replace damaged heart muscle cells and establish new blood vessels to supply them. Discussed here are some of the recent discoveries that feature stem cell replacement and muscle regeneration strategies for repairing the damaged heart.

For those suffering from common, but deadly, heart diseases, stem cell biology represents a new medical frontier. Researchers are working toward using stem cells to replace damaged heart cells and literally restore cardiac function.

Today in the United States, congestive heart failurethe ineffective pumping of the heart caused by the loss or dysfunction of heart muscle cellsafflicts 4.8 million people, with 400,000 new cases each year. One of the major contributors to the development of this condition is a heart attack, known medically as a myocardial infarction, which occurs in nearly 1.1 million Americans each year. It is easy to recognize that impairments of the heart and circulatory system represent a major cause of death and disability in the United States [5].

What leads to these devastating effects? The destruction of heart muscle cells, known as cardiomyocytes, can be the result of hypertension, chronic insufficiency in the blood supply to the heart muscle caused by coronary artery disease, or a heart attack, the sudden closing of a blood vessel supplying oxygen to the heart. Despite advances in surgical procedures, mechanical assistance devices, drug therapy, and organ transplantation, more than half of patients with congestive heart failure die within five years of initial diagnosis. Research has shown that therapies such as clot-busting medications can reestablish blood flow to the damaged regions of the heart and limit the death of cardiomyocytes. Researchers are now exploring ways to save additional lives by using replacement cells for dead or impaired cells so that the weakened heart muscle can regain its pumping power.

How might stem cells play a part in repairing the heart? To answer this question, researchers are building their knowledge base about how stem cells are directed to become specialized cells. One important type of cell that can be developed is the cardiomyocyte, the heart muscle cell that contracts to eject the blood out of the heart’s main pumping chamber (the ventricle). Two other cell types are important to a properly functioning heart are the vascular endothelial cell, which forms the inner lining of new blood vessels, and the smooth muscle cell, which forms the wall of blood vessels. The heart has a large demand for blood flow, and these specialized cells are important for developing a new network of arteries to bring nutrients and oxygen to the cardiomyocytes after a heart has been damaged. The potential capability of both embryonic and adult stem cells to develop into these cells types in the damaged heart is now being explored as part of a strategy to restore heart function to people who have had heart attacks or have congestive heart failure. It is important that work with stem cells is not confused with recent reports that human cardiac myocytes may undergo cell division after myocardial infarction [1]. This work suggests that injured heart cells can shift from a quiescent state into active cell division. This is not different from the ability of a host of other cells in the body that begin to divide after injury. There is still no evidence that there are true stem cells in the heart which can proliferate and differentiate.

Researchers now know that under highly specific growth conditions in laboratory culture dishes, stem cells can be coaxed into developing as new cardiomyocytes and vascular endothelial cells. Scientists are interested in exploiting this ability to provide replacement tissue for the damaged heart. This approach has immense advantages over heart transplant, particularly in light of the paucity of donor hearts available to meet current transplantation needs.

What is the evidence that such an approach to restoring cardiac function might work? In the research laboratory, investigators often use a mouse or rat model of a heart attack to study new therapies (see Figure 9.1. Rodent Model of Myocardial Infarction). To create a heart attack in a mouse or rat, a ligature is placed around a major blood vessel serving the heart muscle, thereby depriving the cardiomyocytes of their oxygen and nutrient supplies. During the past year, researchers using such models have made several key discoveries that kindled interest in the application of adult stem cells to heart muscle repair in animal models of heart disease.

Figure 9.1. Rodent Model of Myocardial Infarction.

( 2001 Terese Winslow, Lydia Kibiuk)

Recently, Orlic and colleagues [9] reported on an experimental application of hematopoietic stem cells for the regeneration of the tissues in the heart. In this study, a heart attack was induced in mice by tying off a major blood vessel, the left main coronary artery. Through the identification of unique cellular surface markers, the investigators then isolated a select group of adult primitive bone marrow cells with a high capacity to develop into cells of multiple types. When injected into the damaged wall of the ventricle, these cells led to the formation of new cardiomyocytes, vascular endothelium, and smooth muscle cells, thus generating de novo myocardium, including coronary arteries, arterioles, and capillaries. The newly formed myocardium occupied 68 percent of the damaged portion of the ventricle nine days after the bone marrow cells were transplanted, in effect replacing the dead myocardium with living, functioning tissue. The researchers found that mice that received the transplanted cells survived in greater numbers than mice with heart attacks that did not receive the mouse stem cells. Follow-up experiments are now being conducted to extend the posttransplantation analysis time to determine the longer-range effects of such therapy [8]. The partial repair of the damaged heart muscle suggests that the transplanted mouse hematopoietic stem cells responded to signals in the environment near the injured myocardium. The
cells migrated to the damaged region of the ventricle, where they multiplied and became “specialized” cells that appeared to be cardiomyocytes.

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9. Can Stem Cells Repair a Damaged Heart? [Stem Cell …

Repairing the heart with stem cells – Harvard Health

Could this experimental treatment reverse damage caused by a heart attack?

The heart muscle relies on a steady flow of oxygen-rich blood to nourish it and keep it pumping. During a heart attack, that blood flow is interrupted by a blockage in an artery. Without blood, the area of heart fed by the affected artery begins to die and scar tissue forms in the area. Over time, this damage can lead to heart failure, especially when one heart attack comes after another.

Though the heart is a tough organ, the damaged portions become unable to pump blood as efficiently as they once could. People who have had a heart attack therefore may face a lifetime of maintenance therapymedications and other treatments aimed at preventing another heart attack and helping the heart work more efficiently.

A new treatment using stem cellswhich have the potential to grow into a variety of heart cell typescould potentially repair and regenerate damaged heart tissue. In a study published last February in The Lancet, researchers treated 17 heart attack patients with an infusion of stem cells taken from their own hearts. A year after the procedure, the amount of scar tissue had shrunk by about 50%.

These results sound dramatic, but are they an indication that we’re getting close to perfecting this therapy? “This is a field where, depending on which investigator you ask, you can get incredibly different answers,” says Dr. Richard Lee, professor of medicine at Harvard Medical School and a leading expert on stem cell therapy.

“The field is young. Some studies show only modest or no improvement in heart function, but others have shown dramatically improved function,” he says. “We’re waiting to see if other doctors can also achieve really good results in other patients.”

Studies are producing such varied outcomes in part because researchers are taking different approaches to harvesting and using stem cells. Some stem cells are taken from the bone marrow of donors, others from the patient’s own heart. It’s not clear which approach is the most promising.

Several different types of approaches are being used to repair damaged heart muscle with stem cells. The stem cells, which are often taken from bone marrow, may be inserted into the heart using a catheter. Once in place, stem cells help regenerate damaged heart tissue.

Like any other therapy, injecting stem cells into the heart can fail or cause side effects. If the stem cells are taken from an unrelated donor, the body’s immune system may reject them. And if the injected cells can’t communicate with the heart’s finely tuned electrical system, they may produce dangerous heart rhythms (arrhythmias). So far, side effects haven’t been a major issue, though, and that has encouraged investigators to push onward.

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Repairing the heart with stem cells – Harvard Health

The Stem Cell Center at Texas Heart Institute

Welcome

The Stem Cell Center Texas Heart Institute is dedicated to the study of adult stem cells and their role in treating diseases of the heart and the circulatory system. Through numerous clinical and preclinical studies, we have come to realize the potential of stem cells to help patients suffering from cardiovascular disease.We are actively enrolling patients in studies using stem cells for the treatment of heart failure, heart attacks, and peripheral vascular disease.

Whether you are a patient looking for information regarding our research, or a doctor hoping to learn more about stem cell therapy, we welcome you to the Stem Cell Center. Please visit our Clinical Trials page for more information about our current trials.

Emerson C. Perin, MD, PhD, FACC Director, Clinical Research for Cardiovascular Medicine Medical Director, Stem Cell Center McNair Scholar

You may contact us at:

E-mail: stemcell@texasheart.org Toll free: 1-866-924-STEM (7836) Phone: 832-355-9405 Fax: 832-355-9440

We are a network of physicians, scientists, and support staff dedicatedto studying stem cell therapy for treating heart disease. Thegoals of the Network are to complete research studies that will potentially lead to more effective treatments for patients with cardiovasculardisease, and to share knowledge quickly with the healthcare community.

Websitein Spanish (En espaol)

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The Stem Cell Center at Texas Heart Institute

Scientists develop cardiac cells using stem cells

For millions of people around the world, who suffer from various diseases, research in stem cells offers a ray of hope. Scientists of the city-based Indian Institute of Science have used stem cells of a mouse to culture cardiac cells.

Explaining the research, Polani B. Seshagiri said their research over the past seven years has helped develop cardiac cells that function and beat in rhythms identical to the original cell.

Speaking on Stem Cell Awareness Day recently, Prof. Seshagiri said stem cells had several advantages and could cure human disorders and diseases, which could not be cured by conventional approaches. However, he warned that there was a need to be aware of the limitations of stem cells.

Sudarshan Ballal, Medical Director, Manipal Health Enterprise, said stem cells had enormous potential as they never die and could be converted into any cell. Stem cells can be converted into organs and maybe years later, organs can be cultivated in labs through stem cell, he said. Elaborating further, he said a stem cell could be compared to a bicycle, which could turn into car, motorbike and spaceship based on the environment and conditions.

Nazeer Ahmed, Deputy Drug Controller of Karnataka, said they were in the process of chalking out regulations for stem cells as there were currently no rules to regulate stem cell research and therapy.

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Scientists develop cardiac cells using stem cells

Guest post: Dr. Gabriele DUva: How to Grow New Heart Cells [The Weizmann Wave]

Dr. Gabriele DUva is finishing up his postdoctoral research at the Weizmann Institute. Here is his account of three years of highly successful research on regenerating heart cells after injury. Among other things, it is the story of the way that different ideas from vastly different research areas can, over the dinner table or in casual conversation, provide the inspiration for outstanding research:

Three years ago, when I joined the lab of Prof. Eldad Tzahor, the emerging field of cardiac regeneration was totally obscure to me. My scientific track at that time was mainly focused on normal and cancer stem cells: cells that build our bodies during development and adulthood. The deregulation of these cells can lead to cancer. I have to admit that I didnt know even the shape of a cardiac cell when my postdoc journey started

Eldads lab was also switching fields well, not drastically, like me, but still it was a transition from a basic research on the development of the heart to the challenge of heart regeneration during adult life.

Two neonatal cardiomyocytes (staining in red) undergoing cell division after treatment with NRG1

In contrast to most tissues in our body, which renew themselves throughout life using our pools of stem cells, the renewal of heart cells in adulthood is extremely low; it almost doesnt exist. Just to give an approximate picture of renewal and regeneration processes: Every day we produce billions of new blood cells that completely replace the old ones in a few months. In contrast, heart cells renewal is so low that, many cardiac cells remain with us for our entire life, from birth to death! Consequently, heart injuries cannot be truly repaired, leading to (often lethal) cardiovascular diseases. This might appear somewhat nonsensical, since the heart is our most vital organ: No (heart) beat no life.

Hence a challenge for many scientists is to understand how to induce heart regeneration Scientists have been trying different strategies, for example, the injection of stem cells. We decided to adopt a different strategy one that mimics the natural regenerative process of healing the heart in such regenerative organisms as amphibians and fish, and even newly-born mice. In all these cases the regeneration of the heart involves the proliferation of heart muscle cells called cardiomyocytes. Therefore the challenge before us was: How can we push cardiomyocytes to divide?

We adopted a team strategy. Cancer turned out to be a somewhat useful model for a strategy. After all, the hallmark of this disease is continuous self-renewal and cell proliferation. Starting from this thought, Prof. Yossi Yarden, a leading expert in the cancer field, suggested: Why dont you try an oncogene, such as ERBB2, whose deregulation can lead to uncontrolled cellular growth and tumour development? The idea was that cardiomyocytes could be pushed into a proliferative state by this cancer-promoting agent. To Eldad, this was a nice life circle closing, since Eldad, when he was a PhD student in Yossis lab, focused exactly on the ERBB2 mechanism of action in cancer progression. I must admit, the idea sounded very intriguing and I really liked it.

Eldad, as a developmental biologist, had a different approach. Based on his field of expertise, his tactic was to apply proliferative (and regenerative) strategies learned from the embryos, when heart cells normally proliferate to form a functional organ. It turned out that a key player in driving embryonic heart growth is again ERBB2!

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Guest post: Dr. Gabriele DUva: How to Grow New Heart Cells [The Weizmann Wave]

In The Future, Spider Silk May Help Grow Your Replacement Heart

Theres been a lot of talk lately about how spider silk is this crazy wonder material that may soon find its way into everything from electronics to ultra-strong fabrics. Now, theres another reason to be excited about spider silk: doctors might one day use the stuff to grow you a new heart.

Growing new organs and tissues outside the body is the bleeding edge of biomedical research. Just imagine: if doctors could grow replacement hearts or kidneys from a patients own stem cells, that patient would no longer have to face the agonizing prospect of waiting to find a suitable donor. The risk of organ rejection would become nil. But theres a lot of R&D to be done before we get there. One initial challenge has been finding a scaffold material to grow organ tissues onsomething thats non-toxic, will not impede cell growth, and will not, itself, be rejected by the body. That, it turns out, is a pretty tall order.

But, as described in a study published recently in PLOS ONE, genetically engineered fibers of spidrointhe protein that builds cobweb strandsmight just fit the bill when it comes to human heart tissue. Spidroin fibers have already proven themselves a useful substrate for growing tendons and cartilages. Researchers at the Moscow Institute for Physics and Technology decided to see whether spidroin grown in the lab via genetically modified yeast cells can also be used to grow cardiomycetes, the cells that form heart tissue.

Heart tissue cells grown on a matrix and stained with fluorescent markers via Alexander Teplenin et al. / PLOS ONE

For their experiments, the researchers seeded a spidroin fiber matrix with neonatal rat cardiomycetes. Within 3 to 5 days, a layer of cardiac cells had formed. Follow-up tests determined that this tissue was able to contract synchronously and conduct electrical impulses, just like normal heart tissue should

Itll probably be some years yet before were growing full human hearts on any sort of artificial scaffold, but its exciting to see that progress is being made toward that goal. If the idea of an artificial heart thats stitched together with spider webs sounds a bit creepy, know this: those fibers are five times stronger than steel and twice as elastic as nylon. If anything, it sounds like an upgrade.

Read the full open-access scientific paper at PLOS ONE.

Top image via Shutterstock

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In The Future, Spider Silk May Help Grow Your Replacement Heart

Mouse's cardiac cells grown in lab

BENGALURU: The day may not be far when organs can be cultured in labs using stem cells. Making a headway in that direction are Indian Institute of Science scientists who have cultured the cardiac cells of a mouse using stem cells.

Stem cells are capable of turning into specific types of cells. “We researched on developing the cardiac cell of a mouse for over seven years. The challenge now is to study how stem cells can be used to produce different organs,” said Polani B Seshagiri on the occasion of Stem Cell Awareness Day on Friday. The professor of IISc’s department of molecular reproduction, development and genetics headed the study.

Polani who has been researching on stem cells for three decades, said these cells offer many advantages in curing human disorders which otherwise aren’t curable using conventional medical approaches. “However, it’s extremely important to be aware of their limitations too,” he added.

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Mouse's cardiac cells grown in lab

Heart Disease Fact Sheet | California’s Stem Cell Agency

CIRM funds many projects seeking to better understand heart disease and to translate those discoveries into new therapies.

If you want to learn more about CIRM funding decisions or make a comment directly to our board, join us at a public meeting. You can find agendas for upcoming public meetings on our meetings page.

Find Out More: Stem Cell FAQ | Stem Cell Videos | What We Fund

Find clinical trials: CIRM does not track stem cell clinical trials. If you or a family member is interested in participating in a clinical trial, please visit clinicaltrials.gov to find a trial near you.

Heart disease strikes in many forms, but collectively it causes one third of all deaths in the U.S. Many forms of heart disease have a common resultcardiomyopathy. While this is commonly called congestive heart failure (CHF), it is really just the heart becoming less efficient due to any number of causes, but the most common is loss of functioning heart muscle due to the damage caused by a heart attack. An estimated 4.8 million Americans have CHF, with 400,000 new cases diagnosed each year. Half die within five years.

Numerous clinical trials are underway testing a type of stem cell found in borne marrow, called mesenchymal stem cells or MSCs, to see if they are effective in treating the form of CHF that follows a heart attack. While those trials have shown some small improvements in patients the researchers have not found that the MSCs are creating replacement heart muscle. They think the improvements may be due to the MSCs creating new blood vessels that then help make the existing heart muscle healthier, or in other ways strengthening the existing tissue.

Californias stem cell agency has numerous awards looking into heart disease (the full list is below). Most of these involve looking for ways to create stem cells that can replace the damaged heart muscle, restoring the hearts ability to efficiently pump blood around the body. Some researchers are looking to go beyond transplanting cells into the heart and are instead exploring the use of tissue engineering technologies, such as building artificial scaffolds in the lab and loading them with stem cells that, when placed in the heart, may stimulate the recovery of the muscle.

Other CIRM-funded researchers are working in the laboratory, looking at stem cells from heart disease patients to better understand the disease and even using those models to discover and test new drugs to see if they are effective in treating heart disease. Other researchers are trying to make a type of specialized heart cell called a pacemaker cell, which helps keep a proper rhythm to the hearts beat.

We also fund projects that are trying to take promising therapies out of the laboratory and closer to being tested in people. These Disease Team Awards encourage the creation of teams that have both the scientific knowledge and business skills needed to produce therapies that can get approval from the Food and Drug Administration (FDA) to be tested in people. In some cases, these awards also fund the early phase clinical trials to show that they are safe to use and, in some cases, show some signs of being effective.

This team developed a way to isolate some heart-specific stem cells that are found in adult heart muscle. They use clumps of cells called Cardiospheres to reduce scarring caused by heart attacks. Initially they used cells obtained from the patients own heart but they later developed methods to obtain the cells they need from donor organs, which allows the procedure to become an off-the-shelf-therapy, meaning it can be available when and where the patient needs it rather than having to create it new each time. The company, working with the Cedars-Sinai team, received FDA approval to begin a clinical trial in June 2012.

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Heart Disease Fact Sheet | California’s Stem Cell Agency

Local innovation repairs holes in the heart

CardioCel has been initially well received with surgeons in Australia and overseas. Photo: Geoff Fisher

For 10 years researchers at Admedus worked day and night trying to work out how to improve soft tissue repair in the human body.

And with the vital help of CSIRO they have been to develop CardioCel, a life-saving heart patch for the repair and reconstruction of cardiovascular defects.

According to the Children’s Heart Foundation, congenital heart disease occurs in one out of 100 births and in at least half of those cases surgery is required and a patch is needed. They state it is the leading cause of birth defect related deaths.

Research undertaken with CSIRO investigated new, potentially ground-breaking applications for CardioCel. The research focused on using stem cells. It found the heart patch has the potential to deliver stem cells and help tissue heal better than other existing products, when used for cardiac repair.

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Derived from animal tissue, the CardioCel patch is engineered over 14 days.

“The first unique feature of this product is that it doesn’t calcify in young patients,” Professor Leon Neethling, Admedus technical director and heart researcher says.

The flexible patch works like human tissue to cover holes in the heart thereby eliminating the need for repeat surgery.

“In the cardiac repair field it has long been recognised that strong, flexible, biocompatible and calcification-resistant tissue scaffolds would be ideal tissues for repair of heart defects,” Admedus’ chief operating officer Dr Julian Chick, says.

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Local innovation repairs holes in the heart

Coalition Duchenne Launches Youtube Interview Series 'Making a Difference in Duchenne'

Newport Beach, California (PRWEB) March 31, 2015

Newport Beach based charity Coalition Duchenne has launched an interview series titled Making a Difference in Duchenne on its Youtube channel (https://www.youtube.com/user/CoalitionDuchenne) focused on individuals making a difference in Duchenne muscular dystrophy research, care, awareness, and education.

The first interview features Dr. Eduardo Marbn MD, PhD, director of the Cedars-Sinai Heart Institute in Los Angeles, talking about cardiac derived stem cells. Dr. Marbn was featured in a November 2011 Economist article Repairing Broken Hearts, read by Coalition Duchenne founder and executive director Catherine Jayasuriya. She lobbied for a focus on Duchenne because cardiac scarring severely compromises the life span of those with the disease. Coalition Duchenne funded successful research applying Marbns stem cell technology to Duchenne. The approach has been clinically proven to mitigate scarring cause by heart attacks. In Marbns therapy, human heart tissue is used to grow specialized heart stem cells, which are injected back into the patients heart.

We need to focus on changing the course of the disease. We lose many young men to cardiac issues. We hope that working with cardiac stem cells is one way we will eventually change that outcome, said Jayasuriya.

The second interview in the Making a Difference in Duchenne series features actor Cody Saintgnue, who plays Brett Talbot in MTVs Teen Wolf. Saintgnue has a unique relationship with Duchenne. He played a young man with muscular dystrophy in his break out role on House MD in 2009. Saintgnue talks about his experience learning to mimic the physicality of a young man with Duchenne, as well as the inspiration he draws from the way those young men overcome many obstacles to live happy, fulfilling lives.

Upcoming interviews will feature: Professor Rachelle Crosbie-Watson from the University of California, Los Angeles, who teaches the first university course focused entirely on Duchenne; Dr. Ron Victor, a Cedars-Sinai cardiologist and researcher looking at the benefits of Cialis and Viagra for Duchenne cardiomyopathy; and, Scotty Bob Morgan, a daredevil wingsuit pilot, who has raised awareness worldwide about Duchenne, flying a specially made Coalition Duchenne wingsuit.

About Duchenne muscular dystrophy: Duchenne muscular dystrophy is a progressive muscle wasting disease. It is the most common fatal disease that affects children. Duchenne occurs in 1 in 3,500 male births, across all races, cultures and countries. Duchenne is caused by a defect in the gene that codes for the protein dystrophin. This is a vital protein that helps connect the muscle fiber to the cell membranes. Without dystrophin, the muscle cells become unstable, are weakened and lose their functionality. Life expectancy ranges from the mid teenage years to the mid 20s. Their minds are unaffected.

About Coalition Duchenne: Jayasuriya founded Coalition Duchenne in 2010 (http://www.coalitionduchenne.org) to raise global awareness for Duchenne muscular dystrophy, to fund research and to find a cure for Duchenne. Coalition Duchenne is a 501c3 non-profit corporation.

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Coalition Duchenne Launches Youtube Interview Series 'Making a Difference in Duchenne'

Heart-on-a-chip beats a steady rhythm

The growing number of biological structures being grown on chips in various laboratories around the world is rapidly replicating the entire gamut of major human organs. Now one of the most important of all a viable functioning heart has been added to that list by researchers at the University of California at Berkeley (UC Berkeley) who have taken adult stem cells and grown a lattice of pulsing human heart tissue on a silicon device.

Sourced from human-induced pluripotent stem cells able to be persuaded into forming many different types of tissue, the human heart device cells are not simply separate groups of cells existing in a petri dish, but a connected series of living cells molded into a structure that is able to beat and react just like the real thing.

“This system is not a simple cell culture where tissue is being bathed in a static bath of liquid,” said study lead author Anurag Mathur, a postdoctoral researcher at UC Berkeley. “We designed this system so that it is dynamic; it replicates how tissue in our bodies actually gets exposed to nutrients and drugs.”

Touted as a possible replacement for living animal hearts in drug-safety screening, the ability to easily access and rapidly analyze a heart equivalent in experiments presents appealing advantages.

“Ultimately, these chips could replace the use of animals to screen drugs for safety and efficacy,” said professor of bioengineering at UC Berkeley, and leader of the research team, Kevin Healy.

The cardiac microphysiological system, as the team calls its heart-on-a-chip, has been designed so that its silicon support structure is equivalent to the arrangement and positioning of conjoining tissue filaments in a human heart. To this supporting arrangement, the researchers loaded the engineered human heart cells into the priming tube, whose cone-shaped funnel assisted in aligning the cells in a number of layers and in one direction.

In this setup, the team created microfluidic channels on each side of the cell holding region to replicate blood vessels to imitate the interchange of nutrients and drugs by diffusion in human tissue. The researchers believe that this arrangement may also one day provide the ability to view and gauge the expulsion of metabolic waste from the cells in future experiments.

“Many cardiovascular drugs target those channels, so these differences often result in inefficient and costly experiments that do not provide accurate answers about the toxicity of a drug in humans,” said Professor Healy. “It takes about US$5 billion on average to develop a drug, and 60 percent of that figure comes from upfront costs in the research and development phase. Using a well-designed model of a human organ could significantly cut the cost and time of bringing a new drug to market.”

The use of animal organs to forecast human reactions to new drugs is problematic, the UC Berkeley researchers note, citing the fundamental differences between species as being responsible for high failure rates in using these models. One aspect responsible for this failure is to be found in the difference in the ion channel structure between human and other animals where heart cells conduct electrical currents at different rates and intensities. It is the standardized nature of using actual human heart cells that the team sees as the heart-on-a-chip’s distinct advantage over animal models.

The UC Berkeley device is certainly not the first replication of an organ-on-a-chip, but potentially one of the first successful ones to integrate living cells and artificial structures in a single functioning unit. Harvard’s spleen-on-a-chip, for example, replicates the operation of the spleen, but does so by using a set of circulatory tubes containing magnetic nanobeads.

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Heart-on-a-chip beats a steady rhythm

Heart-on-a-chip tests drugs cardiotoxicity with its real heartbeat

Lindsey Caldwell

Heart disease is the leading cause of death among Americans. Recently the bio-tech industry has been exploding with cardiac research like last week’s heart attack preventing nanobots. New research by the team at the University of California, Berkley has created working human heart cells on a tiny chip designed to test the efficacy of new drugs in clinical trials. This heart-on-a-chip is officially known as a cardiac microphysiological system, or MPS. Using this heart-on-a-chip, scientists can measure the potential cardiac damage of a drug before it reaches expensive human trials.

Drug trials can take years, and to mitigate risk these drugs undergo testing in non-human subjects. Animals are often used in place of humans, but animal models can be problematic. Specifically, they are less effective at predicting cardiotoxicity, wherein a drug damages the heart. This is important because one-third of drugs withdrawn from testing are pulled due to cardiotoxic effects.

Drugs that are first tested in animal models can succeed to future testing stages without setting off alarms. After successful early stages more time and money is invested and the drugs progress to human trials, only to be stopped in their tracks because they are found to be toxic to human hearts.

The cells on this tiny MPS chip are human heart cells that were created from pluripotent stem cells. These cells react to drugs the same way as a human heart inside a living person. By creating a portable, low-risk, and accurate drug testing environment, scientists may be able to advance clinical trials of new drugs and bring them to market sooner.

Here is a video by the UC Berkley research team of their heart cells actually beating.

Source: Berkeley

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Heart-on-a-chip tests drugs cardiotoxicity with its real heartbeat

Cardiac Stem Cells: Making a Difference in Duchenne – Video



Cardiac Stem Cells: Making a Difference in Duchenne
Dr Eduardo Marban, Director of the Cedars-Sinai Heart Institute, discusses a possible Cardiac Stem Cell breakthrough for Duchenne muscular dystrophy. Coaliti…

By: CoalitionDuchenne

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Cardiac Stem Cells: Making a Difference in Duchenne – Video

The tiny grow-bag that could mend a heart damaged by disease

Coronary heart disease is the countrys leading cause of death A new treatment was designed to treat damaged heart muscle The capsule contains stem cells derived from the patients bone marrow

By Roger Dobson for the Daily Mail

Published: 17:33 EST, 9 March 2015 | Updated: 05:45 EST, 10 March 2015

A new treatment using a tiny grow-bag has been designed to treat damaged heart muscle

A tiny grow-bag could be a new way to mend hearts damaged by disease or heart attack.

The capsule, which is pea-sized, contains stem cells that trigger the growth of new cells.

An estimated 2.3 million people in Britain have coronary heart disease the countrys leading cause of death.

It occurs when the arteries supplying the heart become blocked by fatty substances, reducing the flow of blood.

If a bit of this fatty substance breaks off, it can trigger a blood clot, which in turn cuts off the blood supply to heart muscle, causing it to die off. This is what triggers a heart attack.

Heart disease and heart attacks can also lead to heart failure, where the heart becomes too weak to pump blood around the body properly.

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The tiny grow-bag that could mend a heart damaged by disease

Human heart on a chip could replace animal drug testing

Researchers have created a “heart on a chip” using actual cardiac muscles to help test the effects of heart medication.

Anurag Mathur/Healy Lab

A new device could help make drug testing safer, faster, cheaper — and eliminate the need for animal testing. It’s just an inch long, but inside its silicone body is housed a small piece of cardiac muscle that responds to cardiovascular medications in exactly the same way heart muscle does inside a living human body.

“Ultimately, these chips could replace the use of animals to screen drugs for safety and efficacy,” explained Kevin Healy, UC Berkeley professor of engineering, who led the research team that designed the device.

The problems with using animals to test human heart medication aren’t merely ethical — such concerns about lab animals rarely enter scientific discussions. Rather, there are some serious physiological problems — namely, that drugs designed for humans will not have the same effect on a species that is biologically different from a human.

“These differences often result in inefficient and costly experiments that do not provide accurate answers about the toxicity of a drug in humans,” Healy explained.

“It takes about $5 billion on average to develop a drug, and 60 percent of that figure comes from upfront costs in the research and development phase. Using a well-designed model of a human organ could significantly cut the cost and time of bringing a new drug to market.”

The chips were created using heart muscle grown in a lab from adult human induced pluripotent stem cells — stem cells that can be coaxed to grow into many other types of cell. The team then carefully designed the structure to be similar to the geometry and spacing of connective tissue fibre in a living human heart.

Microfluidic channels carved into the silicone on either side of the cell matrix act the same way as blood vessels, mimicking the exchange of nutrients and drugs with human tissue as it would happen in the body.

The cells start beating on their own within 24 hours of being loaded into the chamber at a healthy resting rate of 55 to 80 beats per minute. In order to test the system, the team then administered four well-known cardiovascular drugs — isoproterenol, E-4031, verapamil and metoprolol. By monitoring the beat rate, the team was able to observe — and accurately predict — the chip’s response to the drugs. Isoproterenol, for example — a drug used to treat slow heart rate — caused the muscle’s beat rate to increase from 55 beats per minute to 124 beats per minute half an hour after being administered.

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Human heart on a chip could replace animal drug testing

Scripps Research, Mayo Clinic scientists find class of drugs that boosts healthy lifespan

IMAGE:Professor Paul Robbins and Associate Professor Laura Niedernhofer led research efforts for the new study at Scripps Florida. view more

Credit: Photo courtesy of The Scripps Research Institute.

JUPITER, FL – March 9, 2015 – A research team from The Scripps Research Institute (TSRI), Mayo Clinic and other institutions has identified a new class of drugs that in animal models dramatically slows the aging process–alleviating symptoms of frailty, improving cardiac function and extending a healthy lifespan.

The new research was published March 9 online ahead of print by the journal Aging Cell.

The scientists coined the term “senolytics” for the new class of drugs.

“We view this study as a big, first step toward developing treatments that can be given safely to patients to extend healthspan or to treat age-related diseases and disorders,” said TSRI Professor Paul Robbins, PhD, who with Associate Professor Laura Niedernhofer, MD, PhD, led the research efforts for the paper at Scripps Florida. “When senolytic agents, like the combination we identified, are used clinically, the results could be transformative.”

“The prototypes of these senolytic agents have more than proven their ability to alleviate multiple characteristics associated with aging,” said Mayo Clinic Professor James Kirkland, MD, PhD, senior author of the new study. “It may eventually become feasible to delay, prevent, alleviate or even reverse multiple chronic diseases and disabilities as a group, instead of just one at a time.”

Finding the Target

Senescent cells–cells that have stopped dividing–accumulate with age and accelerate the aging process. Since the “healthspan” (time free of disease) in mice is enhanced by killing off these cells, the scientists reasoned that finding treatments that accomplish this in humans could have tremendous potential.

The scientists were faced with the question, though, of how to identify and target senescent cells without damaging other cells.

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Scripps Research, Mayo Clinic scientists find class of drugs that boosts healthy lifespan

Scripps Research, Mayo Clinic Scientists Find New Class of Drugs that Dramatically Increases Healthy Lifespan

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Newswise JUPITER, FL March 9, 2015 A research team from The Scripps Research Institute (TSRI), Mayo Clinic and other institutions has identified a new class of drugs that in animal models dramatically slows the aging processalleviating symptoms of frailty, improving cardiac function and extending a healthy lifespan.

The new research was published March 9 online ahead of print by the journal Aging Cell.

The scientists coined the term senolytics for the new class of drugs.

We view this study as a big, first step toward developing treatments that can be given safely to patients to extend healthspan or to treat age-related diseases and disorders, said TSRI Professor Paul Robbins, PhD, who with Associate Professor Laura Niedernhofer, MD, PhD, led the research efforts for the paper at Scripps Florida. When senolytic agents, like the combination we identified, are used clinically, the results could be transformative.

The prototypes of these senolytic agents have more than proven their ability to alleviate multiple characteristics associated with aging, said Mayo Clinic Professor James Kirkland, MD, PhD, senior author of the new study. It may eventually become feasible to delay, prevent, alleviate or even reverse multiple chronic diseases and disabilities as a group, instead of just one at a time.

Finding the Target

Senescent cellscells that have stopped dividingaccumulate with age and accelerate the aging process. Since the healthspan (time free of disease) in mice is enhanced by killing off these cells, the scientists reasoned that finding treatments that accomplish this in humans could have tremendous potential.

The scientists were faced with the question, though, of how to identify and target senescent cells without damaging other cells.

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Scripps Research, Mayo Clinic Scientists Find New Class of Drugs that Dramatically Increases Healthy Lifespan

Bioengineers put human hearts on a chip to aid drug screening

When University of California, Berkeley, bioengineers say they are holding their hearts in the palms of their hands, they are not talking about emotional vulnerability.

Instead, the research team led by bioengineering professor Kevin Healy is presenting a network of pulsating cardiac muscle cells housed in an inch-long silicone device that effectively models human heart tissue, and they have demonstrated the viability of this system as a drug-screening tool by testing it with cardiovascular medications.

This organ-on-a-chip, reported in a study to be published Monday, March 9, in the journal Scientific Reports, represents a major step forward in the development of accurate, faster methods of testing for drug toxicity. The project is funded through the Tissue Chip for Drug Screening Initiative, an interagency collaboration launched by the National Institutes of Health to develop 3-D human tissue chips that model the structure and function of human organs.

“Ultimately, these chips could replace the use of animals to screen drugs for safety and efficacy,” said Healy.

The study authors noted a high failure rate associated with the use of nonhuman animal models to predict human reactions to new drugs. Much of this is due to fundamental differences in biology between species, the researchers explained. For instance, the ion channels through which heart cells conduct electrical currents can vary in both number and type between humans and other animals.

“Many cardiovascular drugs target those channels, so these differences often result in inefficient and costly experiments that do not provide accurate answers about the toxicity of a drug in humans,” said Healy. “It takes about $5 billion on average to develop a drug, and 60 percent of that figure comes from upfront costs in the research and development phase. Using a well-designed model of a human organ could significantly cut the cost and time of bringing a new drug to market.”

The heart cells were derived from human-induced pluripotent stem cells, the adult stem cells that can be coaxed to become many different types of tissue.

The researchers designed their cardiac microphysiological system, or heart-on-a-chip, so that its 3-D structure would be comparable to the geometry and spacing of connective tissue fiber in a human heart. They added the differentiated human heart cells into the loading area, a process that Healy likened to passengers boarding a subway train at rush hour. The system’s confined geometry helps align the cells in multiple layers and in a single direction.

Microfluidic channels on either side of the cell area serve as models for blood vessels, mimicking the exchange by diffusion of nutrients and drugs with human tissue. In the future, this setup could also allow researchers to monitor the removal of metabolic waste products from the cells.

“This system is not a simple cell culture where tissue is being bathed in a static bath of liquid,” said study lead author Anurag Mathur, a postdoctoral scholar in Healy’s lab and a California Institute for Regenerative Medicine fellow. “We designed this system so that it is dynamic; it replicates how tissue in our bodies actually gets exposed to nutrients and drugs.”

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Bioengineers put human hearts on a chip to aid drug screening

This Heart-on-a-Chip Beats Like the Real Thing

Though it may not look at all like the muscle in your chest, this heart-on-a-chip can beat like the real thing. A blend of microfluidics and biological cells, the device will be used as a more efficient means of testing for drug toxicity.

Developed by a team of bioengineers form University of California, Berkeley, the device is designed to mimic the geometry of fibers in a human heart. Pluripotent stem cellsthe cells that can be nudged to become one of the many different types of tissue present in our bodiesare introduced to a channel which is specially designed to encourage cells to grow in multiple layers in one direction, like real cardiac tissue. Here, they grow in to heart cells.

This section is then perfused with blood from microfluidic channels which act as blood vessels. Within 24 hours of lining the structure with heart cells, the structure began to beat at rate of between 55 to 80 beats per minutejust like a real human heart. Anurag Mathur, one of the researchers, explains to PhysOrg:

“This system is not a simple cell culture where tissue is being bathed in a static bath of liquid. We designed this system so that it is dynamic; it replicates how tissue in our bodies actually gets exposed to nutrients and drugs.”

The system has already been used to test established cardiovascular drugs such as isoproterenol, E-4031, verapamil and metoprolol. The team observed effects upon the heart-on-a-chip consistent with those brought about in real humanso, drugs intended to speed up heart rate did exactly that to the cells in the device. The findings are published in Scientific Reports.

It’s hoped that the device will be used to screen drugs, model human genetic diseasesand perhaps even link up with other organs-on-a-chip to predict whole-body reactions too. [Scientific Reports via PhysOrg]

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This Heart-on-a-Chip Beats Like the Real Thing

Study Shows Stem Cells Have Potential to Help Kids Hearts, Too

Durham, NC (PRWEB) February 27, 2015

Several studies showing the promise of stem cells for treating patients with heart failure have made headline news recently. However, all these studies dealt with adult patients only. New research appearing in this months STEM CELLS Translational Medicine shows that stem cells may have the same potential in treating children with congenital heart diseases that can lead to heart failure.

The study, undertaken by researchers at the Mayo Clinic in Rochester, Minn., looked at the feasibility and long-term safety of injecting autologous umbilical cord blood cells directly into the heart muscle at the pediatric stage of heart development. The study was conducted on pigs, due to their hearts similarity to human hearts.

The team injected the stem cells directly into the right ventricle of groups of three- and four-week old healthy piglets, and then compared the results to a control group that did not receive any cells. Over the next three months, the animals were monitored to assess cardiac performance and rhythm to determine how safe the procedure would be for humans.

During this follow-up period, we found no significant acute or chronic cardiac injury pattern caused by the injections directly into the heart, said lead author Timothy J. Nelson, M.D., Ph.D., of the Mayo Clinics Department of Medicine, and all the animals hearts appeared to be normal and healthy.

This led us to conclude that autologous stem cells from cord blood can be safely collected and surgically delivered to children. The study also establishes the foundation for cell-based therapy for children and aims to accelerate the science toward clinical trials for helping children with congenital heart disease that could benefit from a regenerative medicine strategy, he added.

The lead author, Susan Cantero Peral, M.D., Ph.D. commented, This work highlights the importance and utility of umbilical cord blood as it can be applied to new applications. Rather than discarding this sample at birth, individuals with congenital heart disease may one day be able to have these cells collected and processed in a specialized way to make them available for cardiac regeneration.

This work was funded by the Todd and Karen Wanek Family Program for Hypoplastic Left Heart Syndrome founded at the Mayo Clinic.

These data help establish the foundation of a cell-based therapy for juvenile hearts by showing that injections of autologous cells from cord blood are safe and feasible, said Anthony Atala, M.D., editor of STEM CELLS Translational Medicine and director of the Wake Forest Institute for Regenerative Medicine.

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Study Shows Stem Cells Have Potential to Help Kids Hearts, Too

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