Constitutive L-Sox5 overexpression delays differentiation of ATDC5 cells into chondrocytes and correlates with reduced expression of differentiation markers

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• 作者：Dongmei Sun (1)
  Vishwa Deepak (2)
  Ping Mu (1)
  Haiying Jiang (1)
  Xiuming Shi (1)
  Zhongbo Liu (1)
  Xianlu Zeng (1)
  Wenguang Liu (1) (3)
  
  1. Key Laboratory of Molecular Epigenetics of Ministry of Education of China ; Northeast Normal University ; Renmin Street 5268 ; Changchun ; 130024 ; Jilin ; China
  2. Department of Physiology ; Faculty of Health Sciences ; School of Medicine ; University of Pretoria ; Private Bag X323 ; Arcadia ; Pretoria ; 0007 ; South Africa
  3. Institute of Genetics and Cell Biology ; Northeast Normal University ; Changchun ; Jilin ; China
  
• 关键词：L ; Sox5 ; Chondrogenesis ; Runx2 ; Hypertrophy ; Asporin ; Osteoarthritis
• 刊名：Molecular and Cellular Biochemistry
• 出版年：2015
• 出版时间：March 2015
• 年：2015
• 卷：401
• 期：1-2
• 页码：21-26
• 全文大小：1,130 KB
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  4. Lefebvre V, Li P, de Crombrugghe B (1998) A new long form of Sox5 (L-Sox5), Sox6 and Sox9 are coexpressed in chondrogenesis and cooperatively activate the type II collagen gene. EMBO J 17:5718鈥?733 CrossRef
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• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Life Sciences
  Biochemistry
  Medical Biochemistry
  Oncology
  Cardiology
  
• 出版者：Springer Netherlands
• ISSN：1573-4919

文摘

L-Sox5 is a member of sex-determining region Y-type high mobility group box (SOX) family of transcription factors. We assessed the effects of retroviral overexpression of L-Sox5 on chondrocyte differentiation using the clonal murine cell line ATDC5. We observed a temporal-restricted expression pattern of L-Sox5 in insulin-induced ATDC5 cells differentiating toward chondrocyte lineage. The protein expression levels of L-Sox5 showed a drastic decrease in contrast to unaltered mRNA levels during differentiation. L-Sox5 delayed the differentiation of ATDC5 cells as evidenced by Alcian blue staining for proteoglycan synthesis. The mRNA levels of chondrocyte and hypertrophic/osteoarthritic markers were markedly decreased or delayed in L-Sox5 overexpressing cells. L-Sox5 abrogated the promoter activity of Runx2. These results suggest that L-Sox5 protein expression may diminish along with the progress of chondrogenic differentiation. L-Sox5 may act as a negative regulator if expressed aberrantly at least in part by regulating the critical fate of chondrogenesis.