BACKGROUND: Myocardial infarction is a significant cause of heart failure. Currently, therapies are limited and novel revascularization methods may play a role. We investigated the effects of hepatocyte growth factor (HGF) expressed by bone marrow-derived mesenchymal stem cells (MSCs) on post-ischemic heart failure. METHODS: Four weeks after myocardial infarction (MI), Sprague Dawley rats were randomly divided into saline control group, MSC-GFP group, MSC-HGF group, and MSC-HGF+CsA group. After another 4 weeks, hearts were analyzed for ventricular geometry, myocardial function, angiogenesis and endothelial cell density, apoptosis and the expression of calcineurin, Akt, and Bcl-2 protein. RESULTS: In MSC-HGF group, rats exhibited better LV systolic and diastolic function compared with other groups after 8 weeks of MI. Angiogenesis was significantly enhanced by HGF through inducing proliferation of endothelial cells. The effects of HGF on apoptosis were associated with the expression level of calcineurin protein. CONCLUSIONS: Our findings suggest that overexpression of HGF improved ischemic cardiac function through angiogenesis and reduction of apoptosis partly mediated by upregulation of calcineurin.
BACKGROUND:Myocardial infarction is a significant cause of heart failure. Currently, therapies are limited and novel revascularization methods may play a role. We investigated the effects of hepatocyte growth factor (HGF) expressed by bone marrow-derived mesenchymal stem cells (MSCs) on post-ischemic heart failure. METHODS: Four weeks after myocardial infarction (MI), Sprague Dawley rats were randomly divided into saline control group, MSC-GFP group, MSC-HGF group, and MSC-HGF+CsA group. After another 4 weeks, hearts were analyzed for ventricular geometry, myocardial function, angiogenesis and endothelial cell density, apoptosis and the expression of calcineurin, Akt, and Bcl-2 protein. RESULTS: In MSC-HGF group, rats exhibited better LV systolic and diastolic function compared with other groups after 8 weeks of MI. Angiogenesis was significantly enhanced by HGF through inducing proliferation of endothelial cells. The effects of HGF on apoptosis were associated with the expression level of calcineurin protein. CONCLUSIONS: Our findings suggest that overexpression of HGF improved ischemic cardiac function through angiogenesis and reduction of apoptosis partly mediated by upregulation of calcineurin.
Authors: P Locatelli; F D Olea; A Hnatiuk; A De Lorenzi; M Cerdá; C S Giménez; D Sepúlveda; R Laguens; A Crottogini Journal: Gene Ther Date: 2015-03-19 Impact factor: 5.250
Authors: J Raymond Fitzpatrick; John R Frederick; Ryan C McCormick; David A Harris; Ah-Young Kim; Jeffrey R Muenzer; Alex J Gambogi; Jing Ping Liu; E Carter Paulson; Y Joseph Woo Journal: J Thorac Cardiovasc Surg Date: 2010-04-03 Impact factor: 5.209
Authors: Jeremy L Herrmann; Troy A Markel; Aaron M Abarbanell; Brent R Weil; Meijing Wang; Yue Wang; Jiangning Tan; Daniel R Meldrum Journal: Antioxid Redox Signal Date: 2009-08 Impact factor: 8.401