Angiotensin II Increases Expression of Cyclooxygenase-2: Implications for the Function of Vascular Smooth Muscle Cells

doi:10.1124/jpet.102.037705

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Vol. 303, Issue 2, 563-573, November 2002

Angiotensin II Increases Expression of Cyclooxygenase-2: Implications for the Function of Vascular Smooth Muscle Cells

Zhuo-Wei Hu , Reinhold Kerb¹ , Xiao-You Shi , Tzuping Wei-Lavery and Brian B. Hoffman

Geriatric Research, Education, and Clinical Center, Veterans Affairs Palo Alto Health Care System, Palo Alto, California (Z.-W.H., X.-Y.S., T.W.-L., B.B.H.), and the Department of Medicine, Stanford University School of Medicine, Stanford, California (Z.-W.H., R.K., X.-Y.S., T.W.-L., B.B.H.)

In vascular smooth muscle, increased expression of cyclooxygenase-2 (COX-2) has emerged as an important mechanism for regulationof prostanoid synthesis influenced by vessel injury, cytokines,and growth factors. We have investigated how COX-2 participatesin angiotensin II (ANG II)-mediated cell responses in culturedhuman vascular smooth muscle cells (VSMCs). ANG II type 1 (AT1)receptors induce increased accumulation of COX-2, both at themRNA and protein levels. ANG II increased transcription of theCOX-2 gene; also, nuclear extracts from stimulated cells had increasedNF- $kappa$ B binding to its DNA consensus sequence. ANG II-induced COX-2expression was markedly blunted by inhibition of mitogen-activatedprotein kinase. Furthermore, the ANG II-induced increase in COX-2protein abundance was attenuated by both the peroxisome proliferator-activatedreceptor $alpha$ (PPAR $alpha$ ) activator Wy-14,643 [pyrinixic acid; 4-chloro-6-(2,3-xylidino)-2-pyrimidinyl)thioacetic acid] and the PPAR $gamma$ activator 15d-PGJ2 (15-deoxy- $Delta$ ^12-14-prostaglandin J2). Not only did ANG II increase COX-2 expressionand prostaglandin synthesis, ANG II-stimulated DNA synthesis andcell migration were dependent on COX-2 activity. PPAR $alpha$ and PPAR $gamma$ activators inhibited ANG II-stimulated DNA synthesis and cellmigration. These results suggest that ANG II enhances COX-2 expressionat the transcription level; also, COX-2 activity plays an importantrole in mediating ANG II- induced proliferation and migrationof VSMCs, suggesting the possibility of magnification of ANG IIeffects over time due to the induction of COX-2 expression. Theseresults also demonstrate that both the $alpha$ and $gamma$ type of PPAR activatorsinhibit COX-2 expression induced by angiotensin II in VSMCs whichmay have therapeutic significance in vasculardiseases.

¹ Current address: Epidauros Biotechnologie AG, Munich,Germany.

0022-3565/02/3032-0563$00.00/0
THE JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
Copyright © 2002 by U.S. Government

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