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SDF ‐1 promotes ox‐ LDL induced vascular smooth muscle cell proliferation
Author(s) -
Li LingXing,
Zhang XianFeng,
Bai Xue,
Tong Qian
Publication year - 2013
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.10126
Subject(s) - pyrrolidine dithiocarbamate , apoptosis , vascular smooth muscle , cell growth , chemistry , stromal cell , flow cytometry , protein kinase c , cell , medicine , microbiology and biotechnology , endocrinology , signal transduction , biology , nf κb , biochemistry , smooth muscle
The mechanism of the regulatory roles of stromal cell derived factor‐1 (SDF‐1)/C‐X‐C motif receptor 4 (CXCR4) on cell proliferation and apoptosis in vascular smooth muscle cells (VSMCs) via the protein kinase C (PKC) and nuclear factor‐kappa B (NF‐κB) signalling pathways have been investigated. Rat aortic VSMCs were treated with control or an oxidised low‐density lipoprotein (ox‐LDL) atherosclerosis (AS) model. Cells exposed to the AS model were treated with SDF‐1 plus inhibitors specific for PKC (Ro31‐8220), CXCR4 (12G5) or NF‐κB (pyrrolidine dithiocarbamate, PDTC). Cell proliferation was measured with 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT) assay, and apoptosis by flow cytometry. NF‐κB protein expression was analysed using Western blotting. The proliferation rate in the AS model group was significantly higher than the control group, but lower than the SDF‐1 group ( P < 0.05). Apoptosis in the AS model group (ox‐LDL) was significantly higher than the normal control group ( P < 0.05). In addition, the apoptosis rate in the SDF‐1 group was significantly lower than the normal control group ( P < 0.05); however, there was no difference from the Ro31‐8220 group. NF‐κB protein expression in the SDF‐1 group was significantly higher than the AS model (ox‐LDL) group ( P < 0.05). In conclusion, SDF‐1 can promote the proliferation of VSMCs induced by ox‐LDL and inhibit cell apoptosis, via the SDF‐1/CXCR4 axis.