Journal
FRONTIERS IN PHARMACOLOGY
Volume 11, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fphar.2020.01193
Keywords
hypoxia-inducible factor-1 alpha; basic fibroblast growth factor (FGF2); ischemic cardiomyopathy; angiogenesis; antiapoptosis
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Funding
- National Natural Science Foundation of China [81570299, 81570238, 81570342, 81870281]
- Technology Plan Project of Zhejiang Province [WKJ-ZJ-1725]
- Foundation ofWenzhou science and technology bureau [Y20160027]
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Background The combination of antiapoptotic and angiogenic actions may represent a pharmacotherapeutic strategy for the treatment of myocardial infarction. Fibroblast growth factor (FGF) is expressed in various cell types including endothelial and muscle cells and promotes their survival, migration, and proliferation. Methods and Results Myocardial microvascular endothelial cells were divided into four treatment groups, the sham, hypoxia, basic FGF (bFGF), and bFGF plus 2-methoxyestradiol groups, and subjected toin vitroapoptotic analysis and Matrigel assays. Anin vivomodel of myocardial infarction was established by ligaturing the left coronary artery of mice in the four treatment groups. Cardiac performance, myocardial injury, endothelial cell angiogenesis, and myocardial apoptosis were assessed. bFGF administration after myocardial infarction improved cardiac function and cell viability, attenuated myocardial injury and apoptosis, and enhanced angiogenesis. Western blotting of HIF-1 alpha, p-AKT, VEGF, p53, BAX, and Bcl-2 showed that bFGF increased HIF-1 alpha, p-AKT, VEGF, and Bcl-2 and decreased BAX protein levels. Conclusion The results of the present study indicated that bFGF attenuates myocardial injury by inhibiting apoptosis and promoting angiogenesisviaa novel HIF-1 alpha-mediated mechanism and a potential utility of bFGF in protecting against myocardial infarction.
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