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Disease Markers
Volume 2014, Article ID 237067, 9 pages
http://dx.doi.org/10.1155/2014/237067
Research Article

Fluvastatin Upregulates the α1C Subunit of CaV1.2 Channel Expression in Vascular Smooth Muscle Cells via RhoA and ERK/p38 MAPK Pathways

1Fujian Hypertension Research Institute, The First Affiliated Hospital of Fujian Medical University, Fujian 350005, China
2Ultrasound Department, The Second Affiliated People’s Hospital, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350003, China

Received 24 October 2014; Revised 9 December 2014; Accepted 11 December 2014; Published 30 December 2014

Academic Editor: Donald H. Chace

Copyright © 2014 Qiu-Fang Ouyang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Abnormal phenotypic switch of vascular smooth muscle cell (VSMC) is a hallmark of vascular disorders such as atherosclerosis and restenosis. And this process has been related to remodeling of L-type calcium channel (LTCC). We attempted to investigate whether fluvastatin has any effect on VSMC proliferation and LTCC subunit expression as well as the potential mechanisms involved. The VSMCs proliferation was assayed by osteopontin immunofluorescent staining and [3H]-thymidine incorporation. The cell cycle was detected by flow cytometric analysis. The activity of RhoA was determined with pull-down assay. MAPK activity and expression were assessed by western blotting. We demonstrated fluvastatin prevented the VSMCs dedifferentiating into a proliferative phenotype and induced cell cycle arrest in the G0/G1 phase in response to PDGF-BB stimulation. Fluvastatin dose-dependently reversed the downregulation of expression induced by PDGF-BB. Inhibition of ROCK, ERK, or p38 MAPK activation largely enhanced the upregulation effect of fluvastatin . However, blockade of JNK pathway had no effect on expression. We concluded was a VSMC contractile phenotype marker gene. Fluvastatin upregulated expression, at least in part, by inhibiting ROCK, ERK1/2, and p38 MAPK activation. Fluvastatin may be a potential candidate for preventing or treating vascular diseases.