Archive for June, 2019

ABCA4 Retinal Degeneration Autosomal Recessive and Autosomal DominantPlease submit parental samples (no charge) in addition to the patient's sample; requisition needed for each. ABCA4 & ELOVL4 (Leu263 del5tttCTTAA) First Tier Testing$463 12-14 weeks Allele-Specific Testing Followed by Conventional Sequencing 81479 Second Allele Testing$1,611 14-16 weeks Conventional Sequencing 81479AchromatopsiaAutosomal RecessiveCNGA3(exon 8) & CNGB3(Exon 10)First Tier Testing$2338-10 weeksConventional Sequencing81479Autosomal Recessive & X-linkedCNGA3, CNGB3, CNNM4, GNAT2, KCNV2, NBAS, OPN1LW, PDE6C, PDE6H & RPGRExome Testing$220014-16 weeksConventional Sequencing & Next Generation Sequencing81479Autosomal Dominant Neovascular Inflammatory Vitreoretinopathy (ADNIV) Autosomal Dominant CAPN5 $373 12-14 weeks Conventional Sequencing 81479Bardet-Biedl SyndromeAutosomal RecessiveBBS1 (Met390Arg) BBS10 (Leu90 ins1T)First Tier Testing$1408-10 weeksAllele-Specific Testing81479ARL6, BBS1, BBS2, BBS4, BBS5, BBS7, BBS9, BBS10, BBS12, CEP290, INPP5E, LZTFL1, MKS1, MKKS, SDCCAG8, TRIM32 & TTC8Exome Testing$220014-16 weeksAllele-Specific Testing Followed by Conventional Sequencing and Next Generation Sequencing81479Best Disease Autosomal Dominant BEST1 (Full coding region) $373 12-14 weeks Conventional Sequencing 81406Blue Cone Monochromacy X-Linked OPNL1W - Locus Control Region $429 6-8 weeks Deletion Detection (Males Only) 81479Choroideremia X-Linked CHM (Full coding region) $485 14-16 weeks Conventional Sequencing 81479Cone-Rod DystrophyAutosomal DominantCRX (full coding region), GUCA1A(Leu151Phe) & GUCY2D (Exon 13)$2618-10 weeksConventional Sequencing81404, 81479Congenital Stationary Night BlindnessAutosomal Dominant, Autosomal Recessive & X-LinkedCACNA1F, GRM6, PDE6B & TRPM1First Tier Testing$2338-10 weeksConventional Sequencing81479CABP4, CACNA1F, GNAT1, GPR179, GRK1, GRM6, LRIT3, NYX, PDE6B, RDH5, RHO, SAG, SLC24A1, TRPM1Exome Testing$220014-16 weeksConventional Sequencing & Next Generation Sequencing81479Corneal Dystrophy-Stromal Autosomal Dominant TGFBI (Exons 4 & 11-14) $205 12-14 weeks Conventional Sequencing 81479EnhancedS-Cone Syndrome Autosomal RecessivePlease submit parental samples (no charge) in addition to the patient's sample; requisition needed for each. NR2E3 (Exons 2-8) $314 14-16 weeks Conventional Sequencing 81479Jewish Retinal Degeneration Panel - Leber Congenital Amaurosis, Retinitis Pigmentosa and Usher Syndrome Autosomal Recessive DHDDS (Lys42Glu), LCA5 (Gln279Stop), MAK (Lys429 Alu Insertion), PCDH15 (Arg245Stop), USH3A (Asn48Lys) $205 4 weeks Conventional Sequencing 81400, 81479Juvenile Open Angle Glaucoma Autosomal Dominant MYOC (full coding region) $205 12-14 weeks Conventional Sequencing 81479Juvenile X-Linked Retinoschisis X-Linked RS1 (full coding region) $233 10-12 weeks Conventional Sequencing 81479Leber Congenital AmaurosisAutosomal Recessive Please submit parental samples (no charge) in addition to the patient's sample; requisition needed for each.AIPL1, CEP290, CRB1, CRX, GUCY2D, IQCB1, LCA5, LRAT, NMNAT1, RD3, RDH12, RPE65 (entire coding region), RPGRIP1, SPATA7, TULP1First Tier Testing$95714-16 weeksAllele-Specific Testing Followed by Conventional Sequencing81404, 81406, 81408, 81479Exome Testing$28006-8 monthsAllele-Specific Testing Followed by Conventional Sequencing and Next Generation Sequencing81479Leber Hereditary Optic Neuropathy Mitochondrial 3460, 11778, 14484 $140 6-8 weeks Allele-Specific Testing 81401Malattia Leventinese Autosomal Dominant EFEMP1 (Arg345Trp mutation) $140 6-8 weeks Allele-Specific Testing 81479Norrie Disease X-Linked NDP (full coding region) $121 8-10 weeks Conventional Sequencing 81404North Carolina Macular Dystrophy Autosomal Dominant PRDM13, IRX1 $243 6-8 weeks Allele-Specific Testing and Conventional Sequencing 81479Pattern Dystrophy Autosomal Dominant RDS (full coding region) $149 8-10 weeks Conventional Sequencing 81404Primary Open Angle Glaucoma Autosomal Dominant MYOC (full coding region) $205 12-14 weeks Conventional Sequencing 81479Retinitis Pigmentosa Autosomal Dominant C1QTNF5, IMPDH1, MAK, NR2E3, PRPF3, PRPF31, PRPF8, RDH12, RDS, RHO, RP1, RP9, SNRNP200, TOPORS $320 8-10 weeks Allele-Specific Testing Followed by Conventional Sequencing 81404, 81479Retinitis Pigmentosa Autosomal Recessive ABCA4, CC2D2A, CERKL, CLRN1, CNGA1, CRB1, DHDDS, EYS, FAM161A, FLVCR1, IDH3B, IMPG2, LRAT, MAK, NR2E3, NRL, PDE6A, PDE6B, PDE6G, PROM1, RBP3, RDH12, RGR, RLBP1, RPE65, SAG, TTPA, TULP1, USH2A, ZNF513 $833 12 14 weeks Allele-Specific Testing Followed by Conventional Sequencing 81408, 81479Retinitis Pigmentosa X-Linked RP2, RPGR $865 12-14 weeks Conventional Sequencing 81479Sorsby Dystrophy Autosomal Dominant TIMP3 (Exons 1 & 5) $121 8-10 weeks Conventional Sequencing 81479Stargardt like Macular Dystrophy Autosomal Dominant ELOVL4 (Leu263 del5tttCTTAA) $140 6-8 weeks Allele-Specific Testing 81479Stargardt Disease Autosomal Recessive and Autosomal DominantPlease submit parental samples (no charge) in addition to the patient's sample; requisition needed for each. ABCA4 & ELOVL4 (Leu263 del5tttCTTAA) First Tier Testing$463 12-14 weeks Allele-Specific Testing Followed by Conventional Sequencing 81408, 81479 Second Allele Testing$1,611 14-16 weeks Conventional Sequencing 81408, 81479Usher SyndromeAutosomal RecessiveCDH23, CLRN1, MYO7A, PCDH15, USH1C, USH1G & USH2AFirst Tier Testing$5758-10 weeksAllele-Specific Testing Followed by Conventional Sequencing81400, 81407, 81408, 81479Second Allele Testing$575-$1,626 10-12 weeksConventional Sequencing81400, 81407, 81408, 81479ABHD12, CDH23, CIB2, CLRN1, DFNB31, GPR98, HARS, MYO7A, PCDH15, USH1C, USH1G & USH2AExome Testing$220014-16 weeksAllele-Specific Testing Followed by Conventional Sequencing and Next Generation Sequencing81400, 81407, 81408, 81479X-Linked Familial Exudative Vitreoretinopathy (XL-FEVR) X-Linked NDP (full coding region) $121 8-12 weeks Conventional Sequencing 81479

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Genetic Tests Offered (all nonprofit) | The John and ...

Thyroid & BioIdentical Hormone Therapy

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Renewed Vitality - Hormone Replacement Therapy Clinic

JavaScript is disabled on your browser. Please enable JavaScript to use all the features on this page.Highlights

Human iPS cell-derived neural progenitors influence the contractile property of cardiac spheroid.

The contractile function of spheroids depends on the ratio of neural progenitors to cardiac cells.

Neural factors may influence the contractile function of the spheroids.

We havebeen attempting to use cardiac spheroids to construct three-dimensional contractilestructures for failed hearts. Recent studies have reported that neuralprogenitors (NPs) play significant roles in heart regeneration. However, theeffect of NPs on the cardiac spheroid has not yet been elucidated.

This studyaims to demonstrate the influence of NPs on the function of cardiac spheroids.

Thespheroids were constructed on a low-attachment-well plate by mixing humaninduced pluripotent stem (hiPS) cell-derived cardiomyocytes and hiPScell-derived NPs (hiPS-NPs). The ratio of hiPS-NPs was set at 0%, 10%, 20%,30%, and 40% of the total cell number of spheroids, which was 2500. The motionwas recorded, and the fractional shortening and the contraction velocity weremeasured.

Spheroidswere formed within 48 h after mixing the cells, except for the spheroidscontaining 0% hiPS-NPs. Observation at day 7 revealed significant differencesin the fractional shortening (analysis of variance; p=0.01). The bestfractional shortening was observed with the spheroids containing 30% hiPS-NPs.Neuronal cells were detected morphologically within the spheroids under aconfocal microscope.

Theaddition of hiPS-NPs influenced the contractile function of the cardiacspheroids. Further studies are warranted to elucidate the underlying mechanism.

Human iPS cell

Cardiomyocyte

Neural progenitor

Spheroid

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The addition of human iPS cell-derived neural progenitors ...

Cambridge Healthtech Institutes 4th AnnualJune 19-20, 2019

With advances in reprogramming and differentiation technologies, as well as with the recent availability of gene editing approaches, we are finally able to create more complex and phenotypically accurate cellular models based on pluripotent cell technology. This opens new and exciting opportunities for pluripotent stem cell utilization in early discovery, preclinical and translational research. CNS diseases and disorders are currently the main therapeutic area of application with some impressive success stories resulted in clinical trials. Cambridge Healthtech Institutes 4th Annual iPS Cells for Disease Modeling and Drug Discovery conference is designed to bring together experts and bench scientists working with pluripotent cells and end users of their services, researchers working on finding cures for specific diseases and disorders.

Day 1 | Day 2 | Download Brochure | Speaker Biographies

Wednesday, June 19

12:00 pm Registration Open

12:00 Bridging Luncheon Presentation:Structural Maturation in the Development of hiPSC-Cardiomyocyte Models for Pre-clinical Safety, Efficacy, and Discovery

Nicholas Geissse, PhD, CSO, NanoSurface Biomedical

Alec S.T. Smith, PhD, Acting Instructor, Bioengineering, University of Washington

hiPSC-CM maturation is sensitive to structural cues from the extracellular matrix (ECM). Failure to reproduce these signals in vitro can hamper experimental reproducibility and fidelity. Engineering approaches that address this gap typically trade off complexity with throughput, making them difficult to deploy in the modern drug development paradigm. The NanoSurface Car(ina) platform leverages ECM engineering approaches that are fully compatible with industry-standard instrumentation including HCI- and MEA-based assays, thereby improving their predictive power.

12:30 Transition to Plenary

12:50 PLENARY KEYNOTE SESSION

2:20Booth Crawl and Dessert Break in the Exhibit Hall with Poster Viewing

2:25 Meet the Plenary Keynotes

3:05 Chairpersons Remarks

Gabriele Proetzel, PhD, Director, Neuroscience Drug Discovery, Takeda Pharmaceuticals, Inc.

3:10 KEYNOTE PRESENTATION: iPSC-Based Drug Discovery Platform for Targeting Innate Immune Cell Responses

Christoph Patsch, PhD, Team Lead Stem Cell Assays, Disease Relevant Cell Models and Assays, Chemical Biology, Therapeutic Modalities, Roche Pharma Research and Early Development

The role of innate immune cells in health and disease, respectively their function in maintaining immune homeostasis and triggering inflammation makes them a prime target for therapeutic approaches. In order to explore novel therapeutic strategies to enhance immunoregulatory functions, we developed an iPSC-based cellular drug discovery platform. Here we will highlight the unique opportunities provided by an iPSC-based drug discovery platform for targeting innate immune cells.

3:40 Phenotypic Screening of Induced Pluripotent Stem Cell Derived Cardiomyocytes for Drug Discovery and Toxicity Screening

Arne Bruyneel, PhD, Postdoctoral Fellow, Mark Mercola Lab, Cardiovascular Institute, Stanford University School of Medicine

Cardiac arrhythmia and myopathy is a major problem with cancer therapeutics, including newer small molecule kinase inhibitors, and frequently causes heart failure, morbidity and death. However, currentin vitromodels are unable to predict cardiotoxicity, or are not scalable to aid drug development. However, with recent progress in human stem cell biology, cardiac differentiation protocols, and high throughput screening, new tools are available to overcome this barrier to progress.

4:10 Disease Modeling Using Human iPSC-Derived Telencephalic Inhibitory Interneurons - A Couple of Case Studies

Yishan Sun, PhD, Investigator, Novartis Institutes for BioMedical Research (NIBR)

Human iPSC-derived neurons provide the foundation for phenotypic assays assessing genetic or pharmacological effects in a human neurobiological context. The onus is on assay developers to generate application-relevant neuronal cell types from iPSCs, which is not always straightforward, given the diversity of neuronal classes in the human brain and their developmental trajectories. Here we present two case studies to illustrate the use of iPSC-derived telencephalic GABAergic interneurons in neuropsychiatric research.

4:40 Rethinking the Translational The Use of Highly Predictive hiPSC-Derived Models in Pre-Clinical Drug Development

Stefan Braam, CEO, Ncardia

Current drug development strategies are failing to increase the number of drugs reaching the market. One reason for low success rates is the lack of predictive models. Join our talk to learn how to implement a predictive and translational in vitro disease model, and assays for efficacy screening at any throughput.

5:10 4th of July Celebration in the Exhibit Hall with Poster Viewing

5:30 - 5:45 Speed Networking: Oncology

6:05 Close of Day

5:45 Dinner Short Course Registration

6:15 Dinner Short Course*

*Separate registration required.

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Thursday, June 20

7:15 am Registration

7:15 Breakout Discussion Groups with Continental Breakfast

8:10 Chairpersons Remarks

Jeff Willy, PhD, Research Fellow, Discovery and Investigative Toxicology, Vertex

8:15 Levering iPSC to Understand Mechanism of Toxicity

Jeff Willy, PhD, Research Fellow, Discovery and Investigative Toxicology, Vertex

The discovery of mammalian cardiac progenitor cells suggests that the heart consists of not only terminally differentiated beating cardiomyocytes, but also a population of self-renewing stem cells. We recently showed that iPSC cardiomyocytes can be utilized not only to de-risk compounds with potential for adverse cardiac events, but also to understand underlying mechanisms of cell-specific toxicities following xenobiotic stress, thus preventing differentiation and self-renewal of damaged cells.

8:45Pluripotent Stem Cell-Derived Cardiac and Vascular Progenitor Cells for Tissue Regeneration

Nutan Prasain, PhD, Associate Director, Cardiovascular Programs, Astellas Institute for Regenerative Medicine (AIRM)

This presentation will provide the review on recent discoveries in the derivation and characterization of cardiac and vascular progenitor cells from pluripotent stem cells, and discuss the therapeutic potential of these cells in cardiac and vascular tissue repair and regeneration.

9:15 Use of iPSCDerived Hepatocytes to Identify Treatments for Liver Disease

Stephen A. Duncan, PhD, Smartstate Chair in Regenerative Medicine, Professor and Chairman, Department of Regenerative Medicine and Cell Biology, Medical University of South Carolina

MTDPS3 is a rare disease caused by mutations in the DGUOK gene, which is needed for mitochondrial DNA (mtDNA) replication and repair. Patients commonly die as children from liver failure primarily caused by unmet energy requirements. We modeled the disease using DGOUK deficient iPSC derived hepatocytes and performed a screen to identify drugs that can restore mitochondrial ATP production.

9:45Industrial-Scale Generation of Human iPSC-Derived Hepatocytes for Liver-Disease and Drug Development Studies

Liz Quinn, PhD, Associate Director, Stem Cell Marketing, Marketing, Takara Bio USA

Our optimized hepatocyte differentiation protocol and standardized workflow mimics embryonic development and allows for highly efficient differentiation of hPSCs through definitive endoderm into hepatocytes. We will describe the creation of large panels of industrial-scale hPSC-derived hepatocytes with specific genotypes and phenotypes and their utility for drug metabolism and disease modeling.

10:00 Sponsored Presentation (Opportunity Available)

10:15 Coffee Break in the Exhibit Hall with Poster Viewing

10:45 Poster Winner Announced

11:00 KEYNOTE PRESENTATION: Modeling Human Disease Using Pluripotent Stem Cells

Lorenz Studer, MD, Director, Center for Stem Cell Biology, Memorial Sloan Kettering Cancer Center

One of the most intriguing applications of human pluripotent stem cells is the possibility of recreating a disease in a dish and to use such cell-based models for drug discovery. Our lab uses human iPS and ES cells for modeling both neurodevelopmental and neurodegenerative disorders. I will present new data on our efforts of modeling complex genetic disease using pluripotent stem cells and the development of multiplex culture systems.

11:30 Preclinical Challenges for Gene Therapy Approaches in Neuroscience

Gabriele Proetzel, PhD, Director, Neuroscience Drug Discovery, Takeda Pharmaceuticals, Inc.

Gene therapy has delivered encouraging results in the clinic, and with the first FDA approval for an AAV product is now becoming a reality. This presentation will provide an overview of the most recent advances of gene therapy for the treatment of neurological diseases. The discussion will focus on preclinical considerations for gene therapy including delivery, efficacy, biodistribution, animal models and safety.

12:00 pm Open Science Meets Stem Cells: A New Drug Discovery Approach for Neurodegenerative Disorders

Thomas Durcan, PhD, Assistant Professor, Neurology and Neurosurgery, McGill University

Advances in stem cell technology have provided researchers with tools to generate human neurons and develop first-of-their-kind disease-relevant assays. However, it is imperative that we accelerate discoveries from the bench to the clinic and the Montreal Neurological Institute (MNI) and its partners are piloting an Open Science model. By removing the obstacles in distributing patient samples and assay results, our goal is to accelerate translational medical research.

12:30 Elevating Drug Discovery with Advanced Physiologically Relevant Human iPSC-Based Screening Platforms

Fabian Zanella, PhD, Director, Research and Development, StemoniX

Structurally engineered human induced pluripotent stem cell (hiPSC)-based platforms enable greater physiological relevance, elevating performance in toxicity and discovery studies. StemoniXs hiPSC-derived platforms comprise neural (microBrain) or cardiac (microHeart) cells constructed with appropriate inter- and intracellular organization promoting robust activity and expected responses to known cellular modulators.

1:00Overcoming Challenges in CNS Drug Discovery through Developing Translatable iPSC-derived Cell-Based Assays

Jonathan Davila, PhD, CEO, Co-Founder, NeuCyte Inc.

Using direct reprogramming of iPSCs to generate defined human neural tissue, NeuCyte developed cell-based assays with complex neuronal structure and function readouts for versatile pre-clinical applications. Focusing on electrophysiological measurements, we demonstrate the capability of this approach to identify adverse neuroactive effects, evaluate compound efficacy, and serve phenotypic drug discovery.

1:15Enjoy Lunch on Your Own

1:35 Dessert and Coffee Break in the Exhibit Hall with Poster Viewing

1:45 - 2:00 Speed Networking: Last Chance to Meet with Potential Partners and Collaborators!

2:20 Chairpersons Remarks

Gary Gintant, PhD, Senior Research Fellow, AbbVie

2:25 The Evolving Roles of Evolving Human Stem Cell-Derived Cardiomyocyte Preparations in Cardiac Safety Evaluations

Gary Gintant, PhD, Senior Research Fellow, AbbVie

Human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) hold great promise for preclinical cardiac safety testing. Recent applications focus on drug effects on cardiac electrophysiology, contractility, and structural toxicities, with further complexity provided by the growing number of hiPSC-CM preparations being developed that may also promote myocyte maturity. The evolving roles (both non-regulatory and regulatory) of these preparations will be reviewed, along with general considerations for their use in cardiac safety evaluations.

2:55 Pharmacogenomic Prediction of Drug-Induced Cardiotoxicity Using hiPSC-Derived Cardiomyocytes

Paul W. Burridge, PhD, Assistant Professor, Department of Pharmacology, Center for Pharmacogenomics, Northwestern University Feinberg School of Medicine

We have demonstrated that human induced pluripotent stem cell-derived cardiomyocytes successfully recapitulate a patients predisposition to chemotherapy-induced cardiotoxicity, confirming that there is a genomic basis for this phenomenon. Here we will discuss our recent work deciphering the pharmacogenomics behind this relationship, allowing the genomic prediction of which patients are likely to experience this side effect. Our efforts to discover new drugs to prevent doxorubicin-induced cardiotoxicity will also be reviewed.

3:25 Exploring the Utility of iPSC-Derived 3D Cortical Spheroids in the Detection of CNS Toxicity

Qin Wang, PhD, Scientist, Drug Safety Research and Evaluation, Takeda

Drug-induced Central Nervous System (CNS) toxicity is a common safety attrition for project failure during discovery and development phases due low concordance rates between animal models and human, absence of clear biomarkers, and a lack of predictive assays. To address the challenge, we validated a high throughput human iPSC-derived 3D microBrain model with a diverse set of pharmaceuticals. We measured drug-induced changes in neuronal viability and Ca channel function. MicroBrain exposure and analyses were rooted in therapeutic exposure to predict clinical drug-induced seizures and/or neurodegeneration. We found that this high throughput model has very low false positive rate in the prediction of drug-induced neurotoxicity.

3:55 Linking Liver-on-a-Chip and Blood-Brain-Barrier-on-a-Chip for Toxicity Assessment

Sophie Lelievre, DVM, PhD, LLM, Professor, Cancer Pharmacology, Purdue University College of Veterinary Medicine

One of the challenges to reproduce the function of tissues in vitro is the maintenance of differentiation. Essential aspects necessary for such endeavor involve good mechanical and chemical mimicry of the microenvironment. I will present examples of the management of the cellular microenvironment for liver and blood-brain-barrier tissue chips and discuss how on-a-chip devices may be linked for the integrated study of the toxicity of drugs and other molecules.

4:25 Close of Conference

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Arrive early to attend Tuesday, June 18 - Wednesday, June 19

Chemical Biology and Target Validation

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iPS Cells for Disease Modeling and Drug Discovery

Overview of current stem cell-based approaches to treat heart disease

Since heart failure after heart attacks results from death of heart muscle cells, researchers have been developing strategies to remuscularize the damaged heart wall in efforts to improve its function. Researchers are transplanting different types of stem cell and progenitor cells (see above) into patients to repair the damaged heart muscle. These strategies have mainly used either adult stem cells (found in bone marrow, fat, or the heart itself) or pluripotent (ES or iPS) cells.

Preliminary results from experiments with adult stem cells showed that they appeared to improve cardiac function even though they died shortly after transplantation. This led to the idea that these cells can release signals that can improve function without replacing the lost muscle. Clinical trials began in the early 2000s transplanting adult stem cells from the bone marrow and then from the heart. These trials demonstrated that transplanting cells into damaged hearts is feasible and generally safe for patients. However, larger trials that were randomized, blinded, and placebo-controlled, showed fewer indications of improved function. The consensus now is that adult stem cells have modest, if any, benefit to cardiac function.

Research shows that pluripotent stem cell-derived cardiomyocytes can form beating human heart muscle cells that both release the necessary signals and replace muscle lost to heart attack. Transplantation of pluripotent stem cell-derived cardiac cells have demonstrated substantial benefits to cardiac function in animal models of heart disease, from mice to monkeys. Recently, pluripotent stem cell-derived interventions were used in clinical trials for the first time. Patches of human heart muscle cells derived from the stem cells were transplanted onto the surface of failing hearts. Early results suggest that this approach is feasible and safe, but it is too early to know whether there are functional benefits.Research is ongoing to test cellular therapies to treat heart attacks by combining different types of stem cells, repeating transplantations, or improving stem cell patches. Clinical trials using these improved methods are currently targeted to begin around 2020.Unfortunately, many unscrupulous clinics are making unsubstantiated claims about the efficacy of stem cell therapies for heart failure, creating confusion about the current state of cellular approaches for heart failure. To learn more about warning signs of these unproven interventions, please visit Nine Things to Know About Stem Cell Treatments.

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Heart Disease A Closer Look at Stem Cells

JavaScript is disabled on your browser. Please enable JavaScript to use all the features on this page.Abstract

Oxidative stress on transplanted bone marrow-derived mesenchymal stem cells (BMSCs) during acute inflammation is a critical issue in cell therapies. N-acetyl-L cysteine (NAC) promotes the production of a cellular antioxidant molecule, glutathione (GSH). The aim of this study was to investigate the effects of pre-treatment with NAC on the apoptosis resistance and bone regeneration capability of BMSCs. Rat femur-derived BMSCs were treated in growth medium with or without 5mM NAC for 6h, followed by exposure to 100MH2O2 for 24h to induce oxidative stress. Pre-treatment with NAC significantly increased intracellular GSH levels by up to two fold and prevented H2O2-induced intracellular redox imbalance, apoptosis and senescence. When critical-sized rat femur defects were filled with a collagen sponge containing fluorescent-labeled autologous BMSCs with or without NAC treatment, the number of apoptotic and surviving cells in the transplanted site after 3 days was significantly lower and higher in the NAC pre-treated group, respectively. By the 5th week, significantly enhanced new bone formation was observed in the NAC pre-treated group. These data suggest that pre-treatment of BMSCs with NAC before local transplantation enhances bone regeneration via reinforced resistance to oxidative stress-induced apoptosis at the transplanted site.

Acute inflammation

Apoptosis

Cell conditioning

Glutathione

Local transplantation

Senescence

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2018 Elsevier Ltd. All rights reserved.

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Preconditioning of bone marrow-derived mesenchymal stem ...