C-Reactive Protein Upregulates Angiotensin Type 1 Receptors in Vascular Smooth Muscle

• DOI: 10.1161/01.cir.0000061916.95736.e5
• Publication Date: 2003-04-08T01:34:16Z
• Authors: Chao-Hung Wang; Shu-Hong Li; Richard D. Weisel; Paul W.M. Fedak; Aaron S. Dumont; Paul Szmitko; Ren-Ke Li; Donald A.G. Mickle; Subodh Verma
• Keywords: Dichlorofluorescein

Background— Accumulating evidence suggests that C-reactive protein (CRP), in addition to predicting vascular disease, may actively facilitate lesion formation by inciting endothelial cell activation. Given the central importance of angiotensin type 1 receptor (AT -R) pathogenesis atherosclerosis, we examined effects CRP on AT -R expression and kinetics smooth muscle (VSM) cells. In addition, VSM migration, proliferation, reactive oxygen species (ROS) production were evaluated presence absence blocker, losartan. Lastly, (and losartan) neointimal vivo a rat carotid angioplasty model. Methods Results— The human recombinant (0 100 μg/mL) transcript, mRNA stability, studied cultured binding was assessed with 125 I-labeled II (Ang II). migration wound assays, whereas proliferation determined [ 3 H]-incorporation number. Ang II–induced ROS 2′,7′-dichlorofluorescein fluorescence. formation, matrix artery balloon injury markedly upregulated increased number promoted vitro production. Furthermore, potentiated these processes. model, exposure resulted an increase collagen elastin content, expression, as well formation; attenuated Conclusions— CRP, at concentrations known predict cardiovascular events, upregulates -R–mediated atherosclerotic events vivo. These data lend credence notion functions proatherosclerotic factor powerful risk marker.