AUTHOR=Rao Zhiheng , Shen Danping , Chen Jiahui , Jin Lushen , Wu Xueping , Chen Ming , Li Lei , Chu Maoping , Lin Jiafeng 

TITLE=Basic Fibroblast Growth Factor Attenuates Injury in Myocardial Infarction by Enhancing Hypoxia-Inducible Factor-1 Alpha Accumulation

JOURNAL=Frontiers in Pharmacology

VOLUME=11

YEAR=2020

URL=https://www.frontiersin.org/journals/pharmacology/articles/10.3389/fphar.2020.01193

DOI=10.3389/fphar.2020.01193

ISSN=1663-9812

ABSTRACT=<sec><title>Background</title><p>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.</p></sec><sec><title>Methods and Results</title><p>Myocardial microvascular endothelial cells were divided into four treatment groups, the sham, hypoxia, basic FGF (bFGF), and bFGF plus 2-methoxyestradiol groups, and subjected to <italic>in vitro</italic> apoptotic analysis and Matrigel assays. An <italic>in vivo</italic> model 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-1α, p-AKT, VEGF, p53, BAX, and Bcl-2 showed that bFGF increased HIF-1α, p-AKT, VEGF, and Bcl-2 and decreased BAX protein levels.</p></sec><sec><title>Conclusion</title><p>The results of the present study indicated that bFGF attenuates myocardial injury by inhibiting apoptosis and promoting angiogenesis <italic>via</italic> a novel HIF-1α-mediated mechanism and a potential utility of bFGF in protecting against myocardial infarction.</p></sec>