sca-1+ cardiac stem cells mediate acute cardioprotection via paracrine factor sdf-1 following myocardial ischemiareperfusion本来+心脏干细胞调解急性心脏保护通过旁分泌因子sdf-1后心肌ischemiareperfusion.pdfVIP

sca-1+ cardiac stem cells mediate acute cardioprotection via paracrine factor sdf-1 following myocardial ischemiareperfusion本来+心脏干细胞调解急性心脏保护通过旁分泌因子sdf-1后心肌ischemiareperfusion.pdf

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sca-1cardiacstemcellsmediateacutecardioprotectionviaparacrinefactorsdf-1followingmyocardialischemiareperfusion本来心脏干细胞调解急性心脏保护通过旁分泌因子sdf-1后心肌ischemiareperfusion

Sca-1+ Cardiac Stem Cells Mediate Acute Cardioprotection via Paracrine Factor SDF-1 following Myocardial Ischemia/Reperfusion 1 1 2,3 1 1 1 Chunyan Huang , Hongmei Gu , Qing Yu , Mariuxi C. Manukyan , Jeffrey A. Poynter , Meijing Wang * 1 Department of Surgery, Indiana University School of Medicine, Indianapolis, Indiana, United States of America, 2 Department of Pediatrics, Indiana University School of Medicine, Indianapolis, Indiana, United States of America, 3 Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, Indiana, United States of America Abstract Background: Cardiac stem cells (CSCs) promote myocardial recovery following ischemia through their regenerative properties. However, little is known regarding the implication of paracrine action by CSCs in the setting of myocardial ischemia/reperfusion (I/R) injury although it is well documented that non-cardiac stem cells mediate cardioprotection via the production of paracrine protective factors. Here, we studied whether CSCs could initiate acute protection following global myocardial I/R via paracrine effect and what component from CSCs is critical to this protection. Methodology/Principal Findings: A murine model of global myocardial I/R was utilized to investigate paracrine effect of Sca-1+ CSCs on cardiac function. Intracoronary delivery of CSCs or CSC conditioned medium (CSC CM) prior to ischemia significantly improved myocardial function following I/R. siRNA targeting of VEGF in CSCs did not affect CSC-preserved myocardial function in response to I/R injury. However, differentiation of CSCs to cardiomyocytes (DCSCs) abolished this

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