title: Selenoprotein O deficiencies suppress chondrogenic differentiation of ATDC5 cells.
abstract: Selenoprotein O (Sel O) is a selenium-containing protein, but its function is still unclear. In the present study, we observed that the mRNA and protein expression levels of Sel O increased during chondrogenic induction of ATDC5 cells. The effects of Sel O on chondrocyte differentiation were then examined through shRNA-mediated gene silencing technique. The expression of Sel O was significantly suppressed at both mRNA and protein levels in a stable cell line transfected with a Sel O-specific target shRNA construct. Thereafter, we demonstrated that Sel O deficiencies suppress chondrogenic differentiation of ATDC5 cells. Sel O deficiencies inhibited expression of chondrogenic gene Sox9, Col II, and aggrecan. Sel O-deficient cells also accumulated a few cartilage glycosaminoglycans (GAGs) and decreased the activity of alkaline phosphatase (ALP). In addition, Sel O deficiencies inhibited chondrocyte proliferation through delayed cell cycle progression by suppression of cyclin D1 expression. Moreover, Sel O deficiencies induced chondrocyte death through cell apoptosis. In summary, we describe the expression patterns and the essential roles of Sel O in chondrocyte viability, proliferation, and chondrogenic differentiation. Additionally, Sel O deficiency-mediated impaired chondrogenesis may illustrate the mechanisms of Se deficiency in the pathophysiological process of the endemic osteoarthropathy.
authors.affiliation: Department of Human Anatomy, Histology and Embryology, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, 710061, China.
authors.forename: Jidong
authors.initials: J
authors.lastname: Yan
authors.affiliation: College of Life Sciences, Northwest University, Xi'an, Shaanxi, 710069, China.
authors.forename: Yao
authors.initials: Y
authors.lastname: Fei
authors.affiliation: Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Yanta West Road 76, Xi'an, Shaanxi, 710061, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Han
authors.affiliation: Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Yanta West Road 76, Xi'an, Shaanxi, 710061, China. lushemin@xjtu.edu.cn.|Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education of China, Xi'an, China. lushemin@xjtu.edu.cn.
authors.forename: Shemin
authors.initials: S
authors.lastname: Lu
mesh_terms: D017209:Apoptosis / Q000502:physiology; D002356:Cartilage / Q000166:cytology; D002454:Cell Differentiation / Q000502:physiology; D002460:Cell Line; D049109:Cell Proliferation / Q000502:physiology; D002478:Cells, Cultured; D019902:Chondrocytes / Q000166:cytology* / Q000378:metabolism*; D020219:Chondrogenesis; D006025:Glycosaminoglycans / Q000378:metabolism; D006801:Humans; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051140:Selenoproteins / Q000172:deficiency* / Q000235:genetics / Q000378:metabolism
chemical_list: D006025:Glycosaminoglycans; D012333:RNA, Messenger; D051140:Selenoproteins
keywords: ATDC5 cells; Selenoprotein O; cell apoptosis; cell proliferation; chondrocyte differentiation