[The expression and the role of vascular endothelial growth factor (VEGF) in human normal and myocardial infarcted heart].
Coronary collateral vessels reduce the damage of ischemic myocardium after coronary obstruction. Recently, vascular endothelial growth factor (VEGF) has been shown to increase vascular permeability and enhance the endothelial cell growth, leading to neoangiogenesis. VEGF has been reported to be upregulated in some neoplasms with endothelial proliferation, such as glioblastoma and vascularised adenocarcinoma. However, the expression and role of VEGF in human heart and those in its diseased condition have not been investigated. To elucidate its pathophysiological role, we studied the transcription and distribution of VEGF mRNA in normal human and myocardial infarcted hearts. Samples were obtained from 15 autopsy cases with and without ischemic heart disease. VEGF mRNA transcription was examined by using RT-PCR and Southern blot analysis. In all cases VEGF mRNA was detected in atrias, ventricles and valves. The amounts of each VEGF subtypes in cardiomyocytes were different from those in valves. By in situ hybridization method, VEGF mRNA was found in cytoplasm of normal cardiomyocyte but not in the vessels. However, in the cases of acute myocardial infarction, VEGF mRNA was detected in vascular smooth muscle cells of arterioles around the coagulation necrosis of the infarction as well as in mononuclear cells which infiltrated in the granulation tissues. In contrast, VEGF mRNA signals in cardiomyocyte around the necrosis were as much as those in the normal cardiomyocyte in non-diseased areas. By immunohistochemical studies, the mononuclear cells were supposed to be macrophages. This study suggests that VEGF could play an important role in neovascularization in acute myocardial infarction, and suggests that VEGF may have some favorable effect on infarcted myocardium.
Department of Cardiovascular Medicine, Hokkaido University School of Medicine, Sapporo, Japan.
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Shinohara
D000368:Aged; D001483:Base Sequence; D016228:Endothelial Growth Factors / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D004730:Endothelium, Vascular / Q000378:metabolism; D005260:Female; D006801:Humans; D008222:Lymphokines / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D008969:Molecular Sequence Data; D009203:Myocardial Infarction / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism*; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000032:analysis; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors
D016228:Endothelial Growth Factors; D008222:Lymphokines; D012333:RNA, Messenger; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors