期刊
MOLECULAR AND CELLULAR BIOCHEMISTRY
卷 341, 期 1-2, 页码 159-166出版社
SPRINGER
DOI: 10.1007/s11010-010-0447-0
关键词
Atorvastatin; Nur77; Restenosis; Vascular smooth muscle cells; Proliferation; PDGF
类别
It has been reported that Nur77 over-expresses in arteriosclerotic lesions and has both pro- and anti-proliferative effects on vascular smooth muscle cells (VSMCs). We investigated the physiological function of Nur77 on proliferation in VSMCs and the effects of atorvastatin on the expression of Nur77. Platelet-derived growth factor (PDGF), a key growth factor mediating VSMC proliferation in atherogenesis and post-angioplasty restenosis, was employed to induce the transcriptional regulation of Nur77 expression in VSMCs and rat carotid artery post-angioplasty restenosis models were used to investigate the effect of atorvastatin on the expression of Nur77 by immunohistochemistry, RT-PCR, and western blot methods. In cell models, we found that PDGF-B induced Nur77 mRNA expression and protein expression through ERK-MAPK-dependent signaling pathways, and atorvastatin attenuated the expression of Nur77 induced by PDGF-B. In the rat model, our data showed Nur77 was up-regulated in neointima, but down-regulated by atorvastatin. Our results indicate that Nur77 promotes VSMC proliferation, and down-regulation of Nur77 by atorvastatin suggests a novel therapy strategy for atherogenesis based on suppression of VSMC proliferation.
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