title: [Perlecan participates in the protection of ischemic myocardium induced by basic fibroblast growth factor: experiment with rats].
abstract: OBJECTIVE
  To investigate if perlecan (PN) is involved in the myocardial protection of basic fibroblast growth factor (bFGF) in acute myocardial infarction.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Pathophysiology, General Hospital of Chinese People's Liberation Army, Beijing 100853, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Fu
authors.forename: Xiu-hua
authors.initials: XH
authors.lastname: Liu
authors.forename: Xiu-mei
authors.initials: XM
authors.lastname: Zhao
authors.forename: Feng-ying
authors.initials: FY
authors.lastname: Liu
authors.forename: Yu-zhen
authors.initials: YZ
authors.lastname: Li
authors.forename: Fei-fei
authors.initials: FF
authors.lastname: Xu
authors.forename: Sheng
authors.initials: S
authors.lastname: Sun
authors.forename: Li-rong
authors.initials: LR
authors.lastname: Cai
mesh_terms: D000818:Animals; D015153:Blotting, Western; D004195:Disease Models, Animal; D016222:Fibroblast Growth Factor 2 / Q000627:therapeutic use*; D051417:Focal Adhesion Kinase 1 / Q000378:metabolism; D015870:Gene Expression; D019812:Heparan Sulfate Proteoglycans / Q000235:genetics* / Q000502:physiology; D008297:Male; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000201:enzymology / Q000235:genetics; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D020133:Reverse Transcriptase Polymerase Chain Reaction; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
chemical_list: D019812:Heparan Sulfate Proteoglycans; D012333:RNA, Messenger; D016222:Fibroblast Growth Factor 2; C071927:perlecan; D051417:Focal Adhesion Kinase 1; C496052:Ptk2 protein, rat; D048051:p38 Mitogen-Activated Protein Kinases