Stem Cell Treatment Heart Disease

Stem Cells and Heart Disease

Stem Cell Treatments for Heart Disease is an Option

Cardiovascular diseases remain the biggest cause of deaths worldwide, though over the last two decades, cardiovascular mortality rates have declined in many high-income countries but have increased at an astonishingly fast rate in low- and middle-income countries. The percentage of premature deaths from cardiovascular disease range from 4% in high-income countries to 42% in low-income countries. More than 17 million people died from cardiovascular diseases in 2008. Each year, heart disease kills more Americans than cancer. In recent years, cardiovascular risk in women has been increasing and has killed more women than breast cancer.

Measures to prevent cardiovascular disease may include:

  • Keeping unapposed simple carbohydrates under control, no matter what type: fruit, bread, dairy, etc.
  • decrease emotional stress, or how you react to the environment (traffic, work, deadlines, lifestyle, etc.)
  • a low fat high fiber diet including whole grains and plenty of fresh fruit and vegetables (at least five portions a day)
  • a diet high in complex vegetables and colorful fruit
  • tobacco cessation;
  • limit alcohol consumption;
  • lower blood pressures if elevated through diet and exercise;
  • decrease body fat (BMI);
  • increase daily activity to 30 minutes of any kind of exercise per day at least five times per week

A fairly recent emphasis is on the link between low-grade inflammation that hallmarks atherosclerosis and its possible interventions. C-reactive protein (CRP) is a common inflammatory marker that has been found to be present in increased levels in patients at risk for cardiovascular disease. Also osteoprotegerin which is involved with regulation of a key inflammatory transcription factor called NF-κB has been found to be a risk factor of cardiovascular disease and mortality. Studies have shown that Stem Cells have shown the ability to reduce inflammation.


Stem Cell Treatments for Heart Disease is an Option

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Related Articles Stage-specific Effects of Bioactive Lipids on Human iPSC Cardiac Differentiation and Cardiomyocyte Proliferation. Sci Rep. 2018 04 26;8(1):6618 Authors: Sharma A, Zhang Y, Buikema JW, Serpooshan V, Chirikian O, Kosaric N, Churko JM, Dzilic E, Shieh A, Burridge PW, Wu JC, Wu SM Abstract Bioactive lipids such as sphingosine-1-phosphate (S1P) and lysophosphatidic acid (LPA) regulate diverse processes including cell proliferation, differentiation, and migration. However, their roles in cardiac differentiation and cardiomyocyte proliferation have not been explored. Using a 96-well differentiation platform for generating human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) we found that S1P and LPA can independently enhance cardiomyocyte generation when administered at an early stage of differentiation. We showed that the combined S1P and LPA treatment of undifferentiated hiPSCs resulted in increased nuclear accumulation of β-catenin, the canonical Wnt signaling pathway mediator, and synergized with CHIR99021, a glycogen synthase kinase 3 beta inhibitor, to enhance mesodermal induction and subsequent cardiac differentiation. At later stages of cardiac differentiation, the addition of S1P and LPA resulted in cell cycle initiation in hiPSC-CMs, an effect mediated through increased ERK signaling. Although the addition of S1P and LPA alone was insufficient to induce cell division, it was able to enhance β-catenin-mediated hiPSC-CM proliferation. In summary, we demonstrated a developmental stage-specific effect of bioactive lipids to enhance hiPSC-CM differentiation and proliferation via modulating the effect of canonical Wnt/β-catenin and ERK signaling. These findings may improve hiPSC-CM generation for cardiac disease modeling, precision medicine, and regenerative therapies. PMID: 29700394 [PubMed - indexed for MEDLINE]
Related Articles Selective inhibition of receptor activator of NF-κB ligand (RANKL) in hematopoietic cells improves outcome after experimental myocardial infarction. J Mol Med (Berl). 2018 06;96(6):559-573 Authors: Slavic S, Andrukhova O, Ford K, Handschuh S, Latic N, Reichart U, Sasgary S, Bergow C, Hofbauer LC, Kostenuik PJ, Erben RG Abstract The RANK (receptor activator of nuclear factor κB)/RANKL (RANK ligand)/OPG (osteoprotegerin) axis is activated after myocardial infarction (MI), but its pathophysiological role is not well understood. Here, we investigated how global and cell compartment-selective inhibition of RANKL affects cardiac function and remodeling after MI in mice. Global RANKL inhibition was achieved by treatment of human RANKL knock-in (huRANKL-KI) mice with the monoclonal antibody AMG161. huRANKL-KI mice express a chimeric RANKL protein wherein part of the RANKL molecule is humanized. AMG161 inhibits human and chimeric but not murine RANKL. To dissect the pathophysiological role of RANKL derived from hematopoietic and mesenchymal cells, we selectively exchanged the hematopoietic cell compartment by lethal irradiation and across-genotype bone marrow transplantation between wild-type and huRANKL-KI mice, exploiting the specificity of AMG161. After permanent coronary artery ligation, mice were injected with AMG161 or an isotype control antibody over 4 weeks post-MI. MI increased RANKL expression mainly in cardiomyocytes and scar-infiltrating cells 4 weeks after MI. Only inhibition of RANKL derived from hematopoietic cellular sources, but not global or mesenchymal RANKL inhibition, improved post-infarct survival and cardiac function. Mechanistically, hematopoietic RANKL inhibition reduced expression of the pro-inflammatory cytokine IL-1ß in the cardiac cellular infiltrate. In conclusion, inhibition of RANKL derived from hematopoietic cellular sources is beneficial to maintain post-ischemic cardiac function by reduction of pro-inflammatory cytokine production. KEY MESSAGES: Experimental myocardial infarction (MI) augments cardiac RANKL expression in mice. RANKL expression is increased in cardiomyocytes and scar-infiltrating cells after MI. Global or mesenchymal cell RANKL inhibition has no influence on cardiac function after MI. Inhibition of RANKL derived from hematopoietic cells improves heart function post-MI. Hematopoietic RANKL inhibition reduces pro-inflammatory cytokines in scar-infiltrating cells. PMID: 29736604 [PubMed - indexed for MEDLINE]
Related Articles A Thin Layer of Decellularized Porcine Myocardium for Cell Delivery. Sci Rep. 2018 11 01;8(1):16206 Authors: Shah M, Kc P, Copeland KM, Liao J, Zhang G Abstract Decellularized porcine myocardium has shown many benefits as a cell delivery scaffold for cardiac therapy. However, using full thickness decellularized myocardium as cardiac patch may lead to poor viability and inhomogeneous distribution of delivered cells, due to perfusion limitations. In this study, we explored the feasibility of decellularized porcine myocardial slice (dPMS) to construct a vascularized cardiac patch for cell delivery. Decellularized porcine myocardium was sliced into thin layers (thickness~300 µm). Adipose-derived Stem cells (ASCs) obtained from rat and pig were seeded on dPMS. The viability, infiltration, and differentiation of seeded ASCs were examined. The mechanical properties of dPMSs of various thickness and native myocardium were tested. We noticed dPMS supported attachment and growth of rat and pig ASCs. Both rat and pig ASCs showed high viability, similar patterns of proliferation and infiltration within dPMS. Rat ASCs showed expression of early-endothelial markers followed by mature-endothelial marker without any additional inducers on dPMS. Using rat myocardial infarction model, we delivered ASCs using dPMS patched to the infarcted myocardium. After 1 week, a higher number of transplanted cells were present in the infarcted area when cells were delivered using dPMS versus direct injection. Compared with MI group, increased vascular formation was also observed. PMID: 30385769 [PubMed - indexed for MEDLINE]

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