This study was undertaken to assess whether the effect of VLDL on PAI-1 antigen and mRNA induction in Hep G2 cells was influenced by inhibition of the protein kinase C (PKC) signaling pathway. Exposure of HepG2 cells to 100 µg/ml VLDL resulted in a twofold increase in PAI-1 antigen release and total PAI-l mRNA expression. H7 (50 mM) and sphingosine (3-5 mM) almost completely prevented (> 80%) the effects of VLDL on PAI-1 biosynthesis. Similarly down regulation of PKC obtained by previous exposure of cells to PMA, prevented the effect of VLDL on PAI-1. In unstimulated HepG2 cells Gemfibrozil (0.1-0.75 mM) significantly reduced PAI-1 antigen release and mRNA expression. Similarly the drug attenuated PAI-1 biosynthesis in VLDL treated cells, with maximal effect at the 0.75 mM concentration. Interestingly, Bezafibrate failed to affect PAI-1 biosynthesis in both unstimulated and VLDL stimulated cells. It is concluded that VLDL enhance PAI-1 biosynthesis through activation of PKC and that Gemfibrozil, but not Bezafibrate, attenuates PAI-1 induction.

Effects of protein kinase C inhibitors and of gemfibrozil on the biosynthesis of plasminogen activator inhibitor type 1 by HepG2 cells exposed to very low density lipoproteins / C. Banfi, E. Tremoli, L. Sironi, M. Porta, D. Baldassarre, L. Mussoni. ((Intervento presentato al 12. convegno INTERNATIONAL SYMPOSIUM OF DRUG AFFECTING LIPID METABOLISM tenutosi a Houston (Texas) nel 1995.

Effects of protein kinase C inhibitors and of gemfibrozil on the biosynthesis of plasminogen activator inhibitor type 1 by HepG2 cells exposed to very low density lipoproteins

C. Banfi
Primo
;
E. Tremoli
Secondo
;
L. Sironi;D. Baldassarre
Penultimo
;
L. Mussoni
Ultimo
1995

Abstract

This study was undertaken to assess whether the effect of VLDL on PAI-1 antigen and mRNA induction in Hep G2 cells was influenced by inhibition of the protein kinase C (PKC) signaling pathway. Exposure of HepG2 cells to 100 µg/ml VLDL resulted in a twofold increase in PAI-1 antigen release and total PAI-l mRNA expression. H7 (50 mM) and sphingosine (3-5 mM) almost completely prevented (> 80%) the effects of VLDL on PAI-1 biosynthesis. Similarly down regulation of PKC obtained by previous exposure of cells to PMA, prevented the effect of VLDL on PAI-1. In unstimulated HepG2 cells Gemfibrozil (0.1-0.75 mM) significantly reduced PAI-1 antigen release and mRNA expression. Similarly the drug attenuated PAI-1 biosynthesis in VLDL treated cells, with maximal effect at the 0.75 mM concentration. Interestingly, Bezafibrate failed to affect PAI-1 biosynthesis in both unstimulated and VLDL stimulated cells. It is concluded that VLDL enhance PAI-1 biosynthesis through activation of PKC and that Gemfibrozil, but not Bezafibrate, attenuates PAI-1 induction.
Settore BIO/14 - Farmacologia
Effects of protein kinase C inhibitors and of gemfibrozil on the biosynthesis of plasminogen activator inhibitor type 1 by HepG2 cells exposed to very low density lipoproteins / C. Banfi, E. Tremoli, L. Sironi, M. Porta, D. Baldassarre, L. Mussoni. ((Intervento presentato al 12. convegno INTERNATIONAL SYMPOSIUM OF DRUG AFFECTING LIPID METABOLISM tenutosi a Houston (Texas) nel 1995.
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/2434/211502
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