Regulation of plasminogen activator inhibitor activity by plasmin in endothelial cells

Guey Yueh Shi, Shwu Jyh Wang, Bi Ing Chang, Chi Fong Tasi, Ming T. Lin, Wen Chang Chang, Lih Yuh C Wing, Chauyin J. Jen, Hua Lin Wu

研究成果: 雜誌貢獻文章同行評審

6 引文 斯高帕斯(Scopus)


The fibrinolytic activity in endothelial cells was regulated by balance of plasminogen activators and plasminogen activator inhibitors. Plasmin can specifically inhibit the biosynthesis of tissue-type plasminogen activator (t-PA), but not plasminogen activator inhibitor, type 1 (PAI-1) in endothelial cells. The PAI activity in the conditioned medium of endothelial cells was low and remained constant in 24 hours. However, the PAI activity in the conditioned medium of the plasmin-pretreated cells increased linearly in 24 hours. Pretreatment with protein kinase C inhibitors, H-7 or staurosporine, partially suppressed the PAI activity induced by plasmin. Pretreatment of endothelial cells with a G-protein inhibitor pertussis toxin resulted in an inhibition of the plasmin-induced PAI activity. The phospholipase A2 inhibitor mepacrine specifically eliminated the effect of plasmin stimulation on PAI activity. Cyclooxygenase and lipoxygenase inhibitors also partially inhibited the plasmin-stimulated PAI activity in endothelial cells. All these inhibitors did not affect the biosynthesis of the PAI-1 antigen in the presence or absence of plasmin. The results indicate that plasmin increased the PAI activity of endothelial cells via pathways in which protein kinase C, G protein, and phospholipase A2 may be involved.

頁(從 - 到)75-84
期刊Thrombosis Research
出版狀態已發佈 - 1月 1 1996

ASJC Scopus subject areas

  • 心臟病學與心血管醫學
  • 血液學


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