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The expression of p-ATF2 involved in the chondeocytes apoptosis of an endemic osteoarthritis, Kashin-Beck disease.
BMC Musculoskelet Disord. 2013 Jul 16; 14:209.BM

Abstract

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.

Authors

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Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

23866832

Citation

Han, Jing, et al. "The Expression of p-ATF2 Involved in the Chondeocytes Apoptosis of an Endemic Osteoarthritis, Kashin-Beck Disease." BMC Musculoskeletal Disorders, vol. 14, 2013, p. 209.
Han J, Guo X, Tan W, et al. The expression of p-ATF2 involved in the chondeocytes apoptosis of an endemic osteoarthritis, Kashin-Beck disease. BMC Musculoskelet Disord. 2013;14:209.
Han, J., Guo, X., Tan, W., Zhang, F., Liu, J., Wang, W., Xu, P., & Lammi, M. J. (2013). The expression of p-ATF2 involved in the chondeocytes apoptosis of an endemic osteoarthritis, Kashin-Beck disease. BMC Musculoskeletal Disorders, 14, 209. https://doi.org/10.1186/1471-2474-14-209
Han J, et al. The Expression of p-ATF2 Involved in the Chondeocytes Apoptosis of an Endemic Osteoarthritis, Kashin-Beck Disease. BMC Musculoskelet Disord. 2013 Jul 16;14:209. PubMed PMID: 23866832.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The expression of p-ATF2 involved in the chondeocytes apoptosis of an endemic osteoarthritis, Kashin-Beck disease. AU - Han,Jing, AU - Guo,Xiong, AU - Tan,Wuhong, AU - Zhang,Feng, AU - Liu,Jiangtao, AU - Wang,Weizhuo, AU - Xu,Peng, AU - Lammi,Mikko J, Y1 - 2013/07/16/ PY - 2012/12/27/received PY - 2013/07/11/accepted PY - 2013/7/23/entrez PY - 2013/7/23/pubmed PY - 2015/3/31/medline SP - 209 EP - 209 JF - BMC musculoskeletal disorders JO - BMC Musculoskelet Disord VL - 14 N2 - 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. SN - 1471-2474 UR - https://www.unboundmedicine.com/medline/citation/23866832/The_expression_of_p_ATF2_involved_in_the_chondeocytes_apoptosis_of_an_endemic_osteoarthritis_Kashin_Beck_disease_ L2 - https://bmcmusculoskeletdisord.biomedcentral.com/articles/10.1186/1471-2474-14-209 DB - PRIME DP - Unbound Medicine ER -