| Literature DB >> 30054040 |
Jiawei Jiang1, Jinlong Zhang1, Chunshuai Wu1, Xiaofeng Guo1, Chu Chen1, Guofeng Bao1, Yuyu Sun1, Jiajia Chen1, Pengfei Xue1, Guanhua Xu2, Zhiming Cui3.
Abstract
Tumor necrosis factor receptor-associated factor 2 (TRAF2) has been demonstrated that it plays a significant role in cell death receptor signal transduction. The purpose of this study was to investigate the expression of TRAF2 and its possible role in FJOA. We observed an up-regulation of TRAF2 in FJOA by immunohistochemistry and reverse transcription polymerase chain reaction (RT-PCR) compared to normal tissues. In vitro, we used TNF-α to stimulate Human SW1353 chondrosarcoma cells to establish the chondrocytes injury model. Western blot analysis revealed significant expression of TRAF2 and cleaved caspase-3/8 in SW1353 cells. Co-localization of TRAF2/cleaved caspase-3/8 was detected in the cells injury model by double-labeling immunofluorescent staining. We demonstrated a possible anti-apoptotic effect of TRAF2 in chondrocyte apoptosis in FJOA by knockdown of its expression with siRNA. Moreover, TRAF2 knockdown was demonstrated to enhance TNF-α-induced apoptosis by flow cytometry assay. In conclusion, our results show that the up-regulation of TRAF2 may play an important role in the inhibition of chondrocyte apoptosis of FJOA.Entities:
Keywords: Apoptosis; Lumbar facet joint; Osteoarthritis; TRAF2; Tumor necrosis factor-alpha
Mesh:
Substances:
Year: 2018 PMID: 30054040 DOI: 10.1016/j.bbrc.2018.07.096
Source DB: PubMed Journal: Biochem Biophys Res Commun ISSN: 0006-291X Impact factor: 3.575