Pitavastatin suppresses mitogen activated protein kinase-mediated Erg-1 induction in human vascular smooth muscle cells

被引：8

作者：

Lamon, Brian D. ^{[1
]}

Summers, Barbara D. ^{[1
]}

Gotto, Antonio M., Jr. ^{[1
]}

Hajjar, David P. ^{[1
]}

机构：

[1] Cornell Univ, Weill Cornell Med Coll, Ctr Vasc Biol, Dept Pathol & Lab Med, New York, NY 10065 USA

来源：

EUROPEAN JOURNAL OF PHARMACOLOGY | 2009年 / 606卷 / 1-3期

基金：

美国国家卫生研究院;

关键词：

Early growth response (Egr)-1; Statins; Mitogen-activated protein kinase (MAPK); Smooth muscle cells; TISSUE FACTOR EXPRESSION; EARLY GROWTH RESPONSE-1; NF-KAPPA-B; SCAVENGER RECEPTOR; ENDOTHELIAL-CELLS; EGR-1; EXPRESSION; GENE-EXPRESSION; TARGETING EGR-1; IN-VITRO; INJURY;

D O I：

10.1016/j.ejphar.2008.12.047

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Statins have been demonstrated to elicit a broad range of cellular events resulting in an attenuation of the inflammatory response and enhanced protection to the components of the vessel wall. The present study was designed to examine the effect of pitavastatin on pathways associated with the proinflammatory gene, early growth response (Egr)-1 in human vascular smooth muscle cells. Pretreatment with pitavastatin resulted in a dose-dependent reduction in Egr-1 protein and suppressed Egr-1 mRNA expression in response to phorbol 12-myristate 13-acetate (PMA). A reduction in Egr-1 expression reduced the activation of NGFI-A binding protein (NAB)-2, an Egr-1-dependent gene. Furthermore, these events appeared to be dependent on the ability of pitavastatin to attenuate signaling cascades associated with extracellular regulated kinase (ERK) 1/2, but not p38 and c-Jun N-terminal kinase (JNK). (C) 2009 Elsevier B.V. All rights reserved.

引用

页码：72 / 76

页数：5

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