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Originally published In Press as doi:10.1074/jbc.M314172200 on March 3, 2004
J. Biol. Chem., Vol. 279, Issue 19, 20363-20368, May 7, 2004
Angiotensin II Differentially Regulates Interleukin-1- -inducible NO Synthase (iNOS) and Vascular Cell Adhesion Molecule-1 (VCAM-1) Expression
ROLE OF p38 MAPK*
Bingbing Jiang ,
Shanqin Xu,
Xiuyun Hou,
David R. Pimentel, and
Richard A. Cohen
From the
Whitaker Cardiovascular Institute, Vascular Biology Unit, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts 02118
Angiotensin II is implicated in pathophysiological processes associated with vascular injury and repair, which include regulating the expression of numerous NF- B-dependent genes. The present study examined the effect of angiotensin II on interleukin-1 -induced NF-B activation and the subsequent expression of inducible NO synthase (iNOS) and vascular cell adhesion molecule-1 (VCAM-1) in cultured rat vascular smooth muscle cells. Neither NF-B activation nor iNOS or VCAM-1 expression was induced in cells treated with angiotensin II alone. However, when added together with interleukin-1, angiotensin II, through activation of the AT1 receptor, inhibited iNOS expression and enhanced VCAM-1 expression induced by the cytokine. The inhibitory effect of angiotensin II on iNOS expression was associated with a down-regulation of the sustained activation of extracellular signal-regulated kinase (ERK) and NF-B by interleukin-1, whereas the effect on VCAM-1 was independent of ERK activation. The effect of angiotensin II on iNOS was abolished by inhibition of p38 mitogen-activated protein kinase (MAPK) with SB203580, but not by inhibition of PI3 kinase with wortmannin or stress-activated protein kinase/c-Jun NH2-terminal kinase (JNK) with JNK inhibitor II. Thus, angiotensin II, by a mechanism that requires the participation of p38 MAPK, differentially regulates the expression of NF-B-dependent genes in response to interleukin-1 stimulation by controlling the duration of activation of ERK and NF-B.
Received for publication, December 24, 2003
, and in revised form, February 17, 2004.
* This work was supported by National Institutes of Health Grant HL-55620 and American Heart Association Research Award 0160251T. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
 To whom correspondence should be addressed. Tel.: 617-414-1009; Fax: 617-638-7113; E-mail: bjiang{at}bu.edu.
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Copyright © 2004 by the American Society for Biochemistry and Molecular Biology.
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