title: Silencing of osterix expression by siRNA inhibits aldosterone‑induced calcification of vascular smooth muscle cells in mice.
abstract: 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.
authors.affiliation: Department of Hypertension, Shanghai Institute of Hypertension, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, P.R. China.
authors.forename: Yan-Chun
authors.initials: YC
authors.lastname: Gong
authors.affiliation: Department of Hypertension, Shanghai Institute of Hypertension, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, P.R. China.
authors.forename: Yue
authors.initials: Y
authors.lastname: He
authors.affiliation: The Experimental Center of Basic Medicine, Shanghai Medical College, Fudan University, Shanghai 200032, P.R. China.
authors.forename: Hao
authors.initials: H
authors.lastname: Wang
authors.affiliation: Shanghai Key Laboratory of Vascular Biology, Shanghai Institute of Hypertension, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, P.R. China.
authors.forename: Wen-Quan
authors.initials: WQ
authors.lastname: Niu
authors.affiliation: Shanghai Key Laboratory of Vascular Biology, Shanghai Institute of Hypertension, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, P.R. China.
authors.forename: Kai-Da
authors.initials: KD
authors.lastname: Ji
authors.affiliation: Department of Hypertension, Shanghai Institute of Hypertension, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, P.R. China.
authors.forename: Hua
authors.initials: H
authors.lastname: Li
mesh_terms: D000450:Aldosterone / Q000494:pharmacology*; D000818:Animals; D002118:Calcium / Q000378:metabolism; D002478:Cells, Cultured; D015870:Gene Expression; D020868:Gene Silencing; D058574:Integrin-Binding Sialoprotein / Q000235:genetics / Q000378:metabolism; D008297:Male; D051379:Mice; D032389:Myocytes, Smooth Muscle / Q000187:drug effects* / Q000378:metabolism* / Q000473:pathology; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D034741:RNA, Small Interfering / Q000235:genetics*; D000076182:Sp7 Transcription Factor; D014157:Transcription Factors / Q000235:genetics* / Q000378:metabolism; D014162:Transfection; D061205:Vascular Calcification / Q000209:etiology* / Q000473:pathology / Q000628:therapy
chemical_list: C546872:Ibsp protein, mouse; D058574:Integrin-Binding Sialoprotein; D012333:RNA, Messenger; D034741:RNA, Small Interfering; D000076182:Sp7 Transcription Factor; C479466:Sp7 protein, mouse; D014157:Transcription Factors; D000450:Aldosterone; D002118:Calcium