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Int. J. Mol. Sci. 2016, 17(6), 800;

Cardiac Stem Cell Secretome Protects Cardiomyocytes from Hypoxic Injury Partly via Monocyte Chemotactic Protein-1-Dependent Mechanism

Department of Cardiology, Cardiovascular Center, College of Medicine, Korea University, Seoul 02841, Korea
Department of Cardiology, Cardiovascular Center, Korea University Anam Hospital, 73, Inchon-ro, Seongbuk-gu, Seoul 02841, Korea
Author to whom correspondence should be addressed.
Academic Editor: Wenbin Deng
Received: 25 March 2016 / Revised: 10 May 2016 / Accepted: 12 May 2016 / Published: 24 May 2016
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Cardiac stem cells (CSCs) were known to secrete diverse paracrine factors leading to functional improvement and beneficial left ventricular remodeling via activation of the endogenous pro-survival signaling pathway. However, little is known about the paracrine factors secreted by CSCs and their roles in cardiomyocyte survival during hypoxic condition mimicking the post-myocardial infarction environment. We established Sca-1+/CD31− human telomerase reverse transcriptase-immortalized CSCs (Sca-1+/CD31− CSCshTERT), evaluated their stem cell properties, and paracrine potential in cardiomyocyte survival during hypoxia-induced injury. Sca-1+/CD31− CSCshTERT sustained proliferation ability even after long-term culture exceeding 100 population doublings, and represented multi-differentiation potential into cardiomyogenic, endothelial, adipogenic, and osteogenic lineages. Dominant factors secreted from Sca-1+/CD31− CSCshTERT were EGF, TGF-β1, IGF-1, IGF-2, MCP-1, HGF R, and IL-6. Among these, MCP-1 was the most predominant factor in Sca-1+/CD31− CSCshTERT conditioned medium (CM). Sca-1+/CD31− CSCshTERT CM increased survival and reduced apoptosis of HL-1 cardiomyocytes during hypoxic injury. MCP-1 silencing in Sca-1+/CD31− CSCshTERT CM resulted in a significant reduction in cardiomyocyte apoptosis. We demonstrated that Sca-1+/CD31− CSCshTERT exhibited long-term proliferation capacity and multi-differentiation potential. Sca-1+/CD31− CSCshTERT CM protected cardiomyocytes from hypoxic injury partly via MCP-1-dependent mechanism. Thus, they are valuable sources for in vitro and in vivo studies in the cardiovascular field. View Full-Text
Keywords: cardiac stem cells; immortalization; secretome; MCP-1; cardiomyocyte survival cardiac stem cells; immortalization; secretome; MCP-1; cardiomyocyte survival

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Park, C.-Y.; Choi, S.-C.; Kim, J.-H.; Choi, J.-H.; Joo, H.J.; Hong, S.J.; Lim, D.-S. Cardiac Stem Cell Secretome Protects Cardiomyocytes from Hypoxic Injury Partly via Monocyte Chemotactic Protein-1-Dependent Mechanism. Int. J. Mol. Sci. 2016, 17, 800.

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