Perlecan participates in the protection of ischemic myocardium induced by basic fibroblast growth factor: experiment with rats

Abstract

To investigate if perlecan (PN) is involved in the myocardial protection of basic fibroblast growth factor (bFGF) in acute myocardial infarction. Twenty-four Wistar rats were randomized into 3 groups: myocardial infarction group (MI group, n = 8, undergoing ligation of the descending anterior branch of the left coronary artery), bFGF + MI group (n = 10, injected with bFGF into the border myocardium between the infracted and non- infracted areas immediately after the ligation of the descending anterior branch), and sham operation group (n = 6, undergoing sham operation and injection of normal saline). 24 h, 14 days, and 28 days after the operation the hemodynamic parameters, infarct size, and microvessel density (MVD) were observed. The hearts were taken out, RT-PCR was used to detect the mRNA expression of PN, and Western blotting was used to detect the expression of focal adhesion kinase (FAK) and p38 mitogen-activated protein kinase (MAPK) phosphorylation. In the bFGF + MI group, the +dp/dt and -dp/dt were improved markedly, the infarct size was significantly smaller, the MVD value was higher than those of the MI group on day 14 and day 28; the perlecan mRNA expression was higher in the infarct marginal area and interior zone; and the expression of FAK and the p38MAPK phosphorylation were up-regulated in the marginal zone of the bFGF group. bFGF is useful in promoting ischemic myocardial angiogenesis; reducing the size of infracted myocardium, and improving the ventricular function in acute myocardial infarction. Perlecan participates in the cardiac protection induced by bFGF. The relevant pathway is related to up-regulation of FAK and p38MAPK.