Plasminogen activator inhibitor type 1 enhances neointima formation after oxidative vascular injury in atherosclerosis-prone mice | |
Article | |
关键词: E-DEFICIENT MICE; ARTERIAL THROMBOLYSIS; GENE-EXPRESSION; TISSUE FACTOR; THROMBOSIS; LOCALIZATION; PROGRESSION; MIGRATION; APOPTOSIS; RABBITS; | |
DOI : 10.1161/01.CIR.103.25.3105 | |
来源: SCIE |
【 摘 要 】
Background-Plasminogen activator inhibitor type 1 (PAI-1) inhibits neointima formation after vascular injury. Hyperlipidemia modulates the expression of multiple genes, however, and the effects of PAI-I on the arterial response to injury under hyperlipidemic conditions are unknown. The purpose of this study was to examine the impact of PAI-I on intimal hyperplasia and other vascular changes that develop after arterial injury in apolipoprotein E-deficient (apoE(-/-)) mice. Methods and Results-Ferric chloride injury of the midportion of the common carotid arteries of apoE(-/-) mice (n=22) induced formation of a neointima that contained smooth muscle cells, foam cells, neutral lipid, tissue factor, and von Willebrand factor. Interactions between vascular injury and apolipoprotein E deficiency were strongly synergistic; either stimulus alone was insufficient to induce significant neointima formation. Mean intima/media ratios were significantly greater (P<0.03) in apoE(-/-), PAI-1(+/+) mice (5.6
【 授权许可】
Free