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Atherosclerosis. 2007 Aug;193(2):292-8. Epub 2006 Oct 20.

Angiotensin II-induced C-reactive protein generation: inflammatory role of vascular smooth muscle cells in atherosclerosis.

Author information

1
Department of Pharmacology, Xi'an Jiaotong University School of Medicine and Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education, PR China.

Abstract

BACKGROUND:

As the major target of Angiotensin II (Ang II) in the vessel wall, vascular smooth muscle cells (VSMCs) are a tentative source to produce C-reactive protein (CRP). However, it is largely unknown if Ang II is capable of inducing CRP production in VSMCs.

METHODS AND RESULTS:

Ang II induced a concentration-dependent release of CRP in cultured rat VSMCs as measured by sandwich ELISA. Real-time PCR revealed that Ang II significantly upregulated CRP mRNA level in vitro. Ang II-induced CRP generation in aortic VSMCs was also investigated using double-labeled fluorescent immunohistochemistry and in situ hybridization in subchronic Ang II administration in rats. Losartan but not PD123319 markedly blocked the Ang II-induced CRP production in cultured VSMCs, suggesting that such effect was mediated via Ang II type 1 receptor. Further, Western blotting analysis showed that mitogen-activated protein kinase (MAPK) activation was obligatory in Ang II-induced CRP production, since specific MAPK inhibitor PD098059 almost abolished the action.

CONCLUSIONS:

We identified that Ang II is capable of inducing CRP generation in VSMCs, in which Ang II type 1 receptor followed by MAPK signal pathway is involved. It strengthened the role of Ang II-induced CRP production by VSMCs in the inflammatory process in atherosclerosis.

[Indexed for MEDLINE]

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