The expression of p-ATF2 involved in the chondeocytes apoptosis of an endemic osteoarthritis, Kashin-Beck disease

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• 作者：Jing Han (1)
  Xiong Guo (1)
  Wuhong Tan (1)
  Feng Zhang (1)
  Jiangtao Liu (1)
  Weizhuo Wang (2)
  Peng Xu (3)
  Mikko J Lammi (4)
  
• 关键词：JNK and p38 pathways ; ATF2 ; Apoptosis ; Chondrocytes ; Cartilage ; Kashin ; Beck disease
• 刊名：BMC Musculoskeletal Disorders
• 出版年：2013
• 出版时间：December 2013
• 年：2013
• 卷：14
• 期：1
• 全文大小：525KB
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• 作者单位：Jing Han (1)
  Xiong Guo (1)
  Wuhong Tan (1)
  Feng Zhang (1)
  Jiangtao Liu (1)
  Weizhuo Wang (2)
  Peng Xu (3)
  Mikko J Lammi (4)
  
  1. Faculty of Public Health, College Medicine, Key Laboratory of Environment and Gene Related Diseases of Ministry Education, Key Laboratory of Trace elements and Endemic Diseases, Ministry of Health, Xi’an Jiaotong University, 710061, Xi’an, Shaanxi, PR China
  2. Department of Orthopedics Surgery, The Second Affiliated Hospital, College of Medicine,Xi’an Jiaotong University, 710061, Xi’an, Shaanxi, PR China
  3. Department of Orthopaedics Surgery, The Xi’an Red Cross Hospital, 710054, Xi’an, Shaanxi, PR China
  4. Department of Biosciences, Applied Biotechnology, University of Kuopio, Bioteknia 2, 70211, Kuopio, Finland
  

文摘

Background The purpose of the study was to understand the function and expression of ATF2 by JNK and p38 signal pathways in the chondrocytes apoptosis of articular cartilage of the Kashin-Beck disease (KBD). Methods The changes of ATF2, JNK and p38 mRNAs and proteins were investigated between cartilage and chondrocyte as well as KBD and normal. JNK and p38 inhibitors were used as treatments to prevent apoptosis in chondrocytes from KBD patients. Results It was found that the protein levels of p-p38, p-JNK, ATF2 and p-ATF2 increased in KBD human cartilage which is in line with the higher mRNA levels of p38, JNK and ATF2 as compared both with normal cartilage and KBD chondrocytes. In addition, p-ATF2 was only detected in KBD cartilage. Furthermore, JNK inhibitor was more effective than p38 inhibitor in preventing chondrocyte apoptosis at equal concentrations of 10?μM. Conclusion These findings indicated the expression of p-ATF2 by JNK and p38 signal pathways involved in the chondrocyte apoptosis in cartilage with KBD.