Open Access Open Badges Research article

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

Jing Han1, Xiong Guo1*, Wuhong Tan1, Feng Zhang1, Jiangtao Liu1, Weizhuo Wang2, Peng Xu3 and Mikko J Lammi4

Author Affiliations

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

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BMC Musculoskeletal Disorders 2013, 14:209  doi:10.1186/1471-2474-14-209

Published: 16 July 2013



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).


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.


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.


These findings indicated the expression of p-ATF2 by JNK and p38 signal pathways involved in the chondrocyte apoptosis in cartilage with KBD.

JNK and p38 pathways; ATF2; Apoptosis; Chondrocytes; Cartilage; Kashin-Beck disease