Silencing of osterix expression by siRNA inhibits aldosterone-induced calcification of vascular smooth muscle cells in mice

被引:11
作者
Gong, Yan-Chun [1 ]
He, Yue [1 ]
Wang, Hao [2 ]
Niu, Wen-Quan [3 ]
Ji, Kai-Da [3 ]
Li, Hua [1 ]
机构
[1] Shanghai Jiao Tong Univ, Shanghai Inst Hypertens, Ruijin Hosp, Dept Hypertens,Sch Med, 197 Ruijin 2nd Rd, Shanghai 200025, Peoples R China
[2] Fudan Univ, Shanghai Med Coll, Expt Ctr Basic Med, Shanghai 200032, Peoples R China
[3] Shanghai Jiao Tong Univ, Shanghai Inst Hypertens, Ruijin Hosp, Shanghai Key Lab Vasc Biol,Sch Med, Shanghai 200025, Peoples R China
关键词
vascular smooth muscle cell; calcification; siRNA; aldosterone; osterix; TRANSCRIPTION FACTOR OSTERIX; OSTEOBLAST DIFFERENTIATION; AORTIC-VALVE; BONE; DEXAMETHASONE; RAT;
D O I
10.3892/mmr.2016.5484
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The process of vascular calcification shares numerous similarities with that of skeletal mineralization and involves the deposition of hydroxyapatite crystals in arteries and cardiac valves. However, the underlying cellular mechanism remains to be fully elucidated. Microarray analysis in the present study demonstrated that greater than 2,000 genes were upregulated during the calcification of murine vascular smooth muscle cells (VSMCs), of which osterix (OSX) and integrin-binding sialoprotein (IBSP) were the most significantly differentially expressed genes. Following the validation of increased OSX and IBSP expression by reverse transcription-quantitative polymerase chain reaction in calcifying murine VSMCs induced by aldosterone. Subsequent to transfection with siRNA-OSX, results indicated that OSX may inhibit calcification of VSMCs via IBSP. It was suggested that the increased OSX expression in calcifying VSMCs may reflect the well-established prenatal role of OSX. A full understanding of the importance of OSX in this pathological process would improve understanding of the pathogenesis of vascular calcification.
引用
收藏
页码:2111 / 2118
页数:8
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