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Cardiovascular Research Advance Access [Accepted Manuscript] published online on December 3, 2008
Cardiovascular Research, doi:10.1093/cvr/cvn338
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org.

An Essential Role for STIM1 in Neointima Formation Following Arterial Injury

Rui-wei Guo1,*, Hong Wang1,*, Pan Gao1, Mao-Quan Li2, Chun-yu Zeng3, Yang Yu1, Jian-Fei Chen1, Ming-Bao Song1, Yan-kun Shi1 and Lan Huang1

1 Department of Cardiology, Xinqiao hospital, Third military medical university, Chongqing, China. 400037
2 Department of Public Health, Chengdu Medical College, Chengdu, China. 610000
3 Department of Cardiology, Daping hospital, Third military medical university, Chongqing, China. 400037

Corresponding author: Lan Huang, E-mail address:huanglan260{at}126.com, Tel: +86-23-68755601; Fax: +86-23-68755601 Postal address: Department of Cardiology, Xinqiao hospital, Third military medical university, Chongqing, China. 400037

Aim: There is evidence to suggest that stromal interaction molecule 1 (STIM1) functions as a Ca2+ sensor on the endoplasmic reticulum, leading to transduction of signals to the plasma membrane and opening of store-operated Ca2+ channels (SOC). SOC have been detected in vascular smooth muscle cells (VSMCs) and are thought to have an essential role in the regulation of contraction and cell proliferation. We hypothesized that knockdown of STIM1 inhibits VSMC proliferation and suppresses neointimal hyperplasia.

Methods and Results: We examined the effect of the knockdown of STIM1 using a rat balloon injury model and cultured rat aortic VSMCs. Interestingly, knockdown of rat STIM1 by adenovirus delivery of siRNA significantly suppressed neointimal hyperplasia in a rat carotid artery balloon injury model at 14 days after injury. The re-expression of human STIM1 to smooth muscle reversed the effect of STIM1 knockdown on neointimal formation. Rat aortic VSMCs were used for the in vitro assays. Knockdown of endogenous STIM1 significantly inhibited proliferation and migration of VSMCs. Moreover, STIM1 knockdown induced cell-cycle arrest in G0/G1 and resulted in a marked decrease in SOC. Replenishment with recombinant human STIM1 reversed the effect of siRNA knockdown. These results suggest STIM1 has a critical role in neointimal formation in a rat model of vascular injury.

Conclusions: STIM1 may represent a novel therapeutic target in the prevention of restenosis after vascular interventions.

KEYWORDS STIM1; VSMC proliferation; neointimal; vascular injury; restenosis

Time for primary review: 27 Days

* Rui-wei Guo and Hong Wang contributed equally to this work.


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