ArticleAntioxidants & redox signaling2010
Factors Released from Embryonic Stem Cells Stimulate c-kit-FLK-1(+ve) Progenitor Cells and Enhance Neovascularization.
Article in Antioxidants & redox signaling, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 29 citations in OpenAlex.
- The Effect of The Conditioned Medium from Human Embryonic Stem Cells on Mouse Oocytes In Vitro Maturation.Cell journal · 2023Article
- Secreted Frizzled-Related Protein-2 Inhibits Doxorubicin-Induced Apoptosis Mediated through the Akt-mTOR Pathway in Soleus Muscle.Oxidative medicine and cellular longevity · 2018Article
- Generation of electrophysiologically functional cardiomyocytes from mouse induced pluripotent stem cells.Stem cell research · 2016Article
- Fibroblast Growth Factor-9 Activates c-Kit Progenitor Cells and Enhances Angiogenesis in the Infarcted Diabetic Heart.Oxidative medicine and cellular longevity · 2016Article
- Hypoxia-pretreated human MSCs attenuate acute kidney injury through enhanced angiogenic and antioxidative capacities.BioMed research international · 2014Article
- Local activation of cardiac stem cells for post-myocardial infarction cardiac repair.Journal of cellular and molecular medicine · 2012Review
- Article
- Embryonic stem cells improve cardiac function in Doxorubicin-induced cardiomyopathy mediated through multiple mechanisms.Cell transplantation · 2012Article
- MicroRNA-1 transfected embryonic stem cells enhance cardiac myocyte differentiation and inhibit apoptosis by modulating the PTEN/Akt pathway in the infarcted heart.American journal of physiology. Heart and circulatory physiology · 2011Article
- ES cells overexpressing microRNA-1 attenuate apoptosis in the injured myocardium.Molecular and cellular biochemistry · 2011Article
- Induced pluripotent stem (iPS) cells repair and regenerate infarcted myocardium.Molecular pharmaceutics · 2011Article
- TGF-β2 treatment enhances cytoprotective factors released from embryonic stem cells and inhibits apoptosis in infarcted myocardium.American journal of physiology. Heart and circulatory physiology · 2011Article
- Stem and progenitor cells for neurological repair: minor issues, major hurdles, and exciting opportunities for paracrine-based therapeutics.Journal of cellular biochemistry · 2011Review
- Embryonic Stem Cell Conditioned Medium Supports In Vitro Maturation of Mouse Oocytes.Avicenna journal of medical biotechnologyArticle
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
We examined whether factors released from embryonic stem (ES) cells inhibit cardiac and vascular cell apoptosis and stimulate endogenous progenitor cells that enhance neovascularization with improved cardiac function. We generated and transplanted ES-conditioned medium (CM) in the infarcted heart to examine effects on cardiac and vascular apoptosis, activation of endogenous c-kit and FLK-1(+ve) cells, and their role in cardiac neovascularization. TUNEL, caspase-3 activity, immunohistochemistry, H&E, and Masson's trichrome stains were used to determine the effect of transplanted ES-CM on cardiac apoptosis and neovascularization. TUNEL staining and caspase-3 activity confirm significantly (p < 0.05) reduced apoptosis in MI+ES-CM compared with MI+ cell culture medium. Immunohistochemistry demonstrated increased (p < 0.05, 53%) c-kit(+ve) and FLK-1(+ve) positive cells, as well as increased (p < 0.05, 67%) differentiated CD31-positive cells in ES-CM groups compared with respective controls. Furthermore, significantly (p < 0.05) increased coronary artery vessels were observed in ES-CM transplanted hearts compared with control. Heart function was significantly improved following ES-CM transplantation. Next, we observed significantly increased (p < 0.05) levels of c-kit activation proteins (HGF and IGF-1), anti-apoptosis factors (IGF-1 and total antioxidants), and neovascularization protein (VEGF). In conclusion, we suggest that ES-CM following transplantation in the infarcted heart inhibits apoptosis, activates cardiac endogenous c-kit and FLK-1(+ve) cells, and differentiates them into endothelial cells (ECs) that enhances neovascularization with improved cardiac function.
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