Open AccessAn essential role for stromal interaction molecule 1 in neointima formation following arterial injury
Author(s) -
Ruiwei Guo,
Hong Wang,
Pan Gao,
Maoquan Li,
Chunyu Zeng,
Yang Yu,
Jianfei Chen,
Mingbao Song,
Yan-Kun Shi,
Lan Huang
Publication year - 2008
Publication title -
cardiovascular research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.774
H-Index - 219
eISSN - 1755-3245
pISSN - 0008-6363
DOI - 10.1093/cvr/cvn338
Subject(s) - gene knockdown , vascular smooth muscle , stim1 , neointima , neointimal hyperplasia , small interfering rna , microbiology and biotechnology , restenosis , stromal cell , endoplasmic reticulum , cell growth , biology , endocrinology , chemistry , medicine , transfection , cell culture , apoptosis , stent , biochemistry , genetics , smooth muscle
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.
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