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Aldosterone induces C-reactive protein expression via MR-ROS-MAPK-NF-κB signal pathway in rat vascular smooth muscle cells.

Abstract：

:Atherosclerosis is a chronic inflammatory disease in the vessel. As a representative inflammatory cytokine, C-reactive protein (CRP) participates in atherogenesis. Although hyperaldosteronism is known to evoke inflammatory response in several tissues and cell types, there is no direct evidence to demonstrate the proinflammatory effect of aldosterone on vascular smooth muscle cells (VSMCs) through CRP. In this study, we observed the effect of aldosterone on CRP expression and the molecular mechanisms in rat VSMCs. The results showed that aldosterone induced CRP expression in VSMCs in vitro and in vivo. Mineralocorticoid receptor (MR) antagonist spironolactone abolished aldosterone-induced CRP expression. In addition, aldosterone stimulated generation of reactive oxygen species (ROS) and activated ERK1/2 phosphorylation, whereas spironolactone inhibited aldosterone-stimulated ROS generation and ERK1/2 phosphorylation. Antioxidant NAC decreased aldosterone-induced CRP expression and ERK1/2 phosphorylation. The further study confirmed that ERK1/2 inhibitor PD98059 and NF-κB inhibitor pyrrolidine dithiocarbamate both depressed aldosterone-induced CRP expression. These demonstrate that aldosterone is able to induce CRP expression via MR-ROS-ERK1/2-NF-κB signal pathway in VSMCs, which provides a new evidence for the proinflammatory and proatherosclerotic effects of aldosterone.

journal_name

Mol Cell Endocrinol

journal_title

Molecular and cellular endocrinology

authors

Zhang X,Liu J,Pang X,Zhao J,Wang S,Wu D

doi

10.1016/j.mce.2014.08.003

subject

Has Abstract

pub_date

2014-09-01 00:00:00

pages

61-8

issue

1-2

eissn

0303-7207

issn

1872-8057

pii

S0303-7207(14)00237-8

journal_volume

395

pub_type

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