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mediates lipoprotein-induced generation
of PAI-1 from vascular endothelial cells
Departments of Internal Medicine and Physiology, University of Manitoba, Winnipeg, Manitoba, Canada R3E OW3
Elevated levels of low-density lipoproteins (LDL) and
lipoprotein(a) [Lp(a)] have been considered strong risk
factors for atherosclerotic cardiovascular disease. Increased
production of plasminogen activator inhibitor-1 (PAI-1) has been
implicated in the development of thrombosis and atherosclerosis.
Previous studies by our group and others demonstrated that oxidation
enhances LDL- and Lp(a)-induced production of PAI-1 in human umbilical vein endothelial cells (HUVEC). The present study examined the involvement of protein kinase C (PKC) and its isoform in vascular endothelial cells (EC) induced by native or oxidized LDL and Lp(a). Treatment with Lp(a) or LDL transiently increased PKC activity at 15 min and 5.5 h after the start of lipoprotein treatment in EC.
Copper-oxidized LDL and Lp(a) induced greater PKC activation in EC
compared with comparable forms of those lipoproteins. Additions of 1 µM calphostin C, a PKC-specific inhibitor, at the beginning or 
5 h,
but not 9 h, after the initiation of lipoprotein treatment, blocked
native and oxidized LDL- or Lp(a)-induced increases in PKC activity and
PAI-1 production. Treatment of LDL, Lp(a), or their oxidized forms was
induced in translocation of PKC-
1 from cytosol to membrane in HUVEC.
Treatments with 60 nM 379196, a PKC--specific inhibitor, effectively
prevented PAI-1 production induced by LDL, Lp(a), or their oxidized
forms in HUVEC and human coronary artery EC. The results suggest that
activation of PKC- may mediate the production of PAI-1 in cultured
arterial and venous EC induced by LDL, Lp(a), or their oxidized forms.
low-density lipoproteins; lipoprotein(a); oxidation; plasminogen activator inhibitor-1
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