文献类型：期刊文献

英文题名：FSTL1 promotes nitric oxide-induced chondrocyte apoptosis via activating the SAPK/JNK/caspase3 signaling pathway

作者：Xu, Chao[1];Jiang, Tao[2];Ni, Su[3];Chen, Chaoqun[2];Li, Chenkai[3];Zhuang, Chao[4];Zhao, Gongyin[4];Jiang, Shijie[4];Wang, Liangliang[4];Zhu, Ruixia[4];van Wijnen, Andre J.[6];Wang, Yuji[4,5,6]

第一作者：Xu, Chao

通信作者：Wang, YJ[1]

机构：[1]Nanjing Med Univ, 101Longmian Ave, Nanjing 210039, Peoples R China;[2]Nanjing Univ Tradit Chinese Med, Changzhou Tradit Chinese Med Hosp, Dept Orthopaed, 25 Heping North Rd, Changzhou 213003, Jiangsu, Peoples R China;[3]Nanjing Med Univ, Affiliated Changzhou Peoples Hosp 2, Med Res Ctr, 29 Xinglong Alley, Changzhou 213003, Jiangsu, Peoples R China;[4]Nanjing Med Univ, Affiliated Changzhou Peoples Hosp 2, Dept Orthoped, 29 Xinglong Alley, Changzhou 213003, Jiangsu, Peoples R China;[5]Gansu Univ Chinese Med, Affiliated Hosp 3, Dept Orthoped, 222 Silong Rd, Baiyin 730900, Peoples R China;[6]Mayo Clin, Dept Orthoped Surg & Biochem & Mol Biol, Rochester, MN USA

第一机构：Nanjing Med Univ, 101Longmian Ave, Nanjing 210039, Peoples R China

通信机构：[1]corresponding author), Nanjing Med Univ, Affiliated Changzhou Peoples Hosp 2, Dept Orthoped, 29 Xinglong Alley, Changzhou 213003, Jiangsu, Peoples R China.

年份：2020

卷号：732

外文期刊名：GENE

收录：;Scopus(收录号：2-s2.0-85078207253);WOS:【SCI-EXPANDED(收录号:WOS:000515209200003)】；

基金：This work was supported by grants from the National Natural Science Foundation of China (81171680 to Y.W.), the Social Development project of Jiangsu province, China (BE2015632 to Y.W.), the Natural Science Foundation of the Jiangsu for Youth, China (BK20180182 to S.N.), the Changzhou Science and Technology Program, China (CJ20180057 to S.N.), the Changzhou Science and Technology Program, China (QN201930 to C.L.) and China Postdoctoral Science Foundation (2019M651898 to S.N.)

语种：英文

外文关键词：Follistatin-like protein I; Apoptosis; Chondrocytes; Osteoarthritis

摘要：Objective: Previous studies have shown that follistatin-like protein 1 (FSTL1) is elevated in the synovial fluid of osteoarthritis and is associated with disease activity. The experiment was performed to stuy the effect and mechanism of FSTL1 on chondrocyte apoptosis in osteoarthritis. Design: After the isolation of human normal and osteoarthritis (OA) chondrocytes, the expression of FSTL1 was detected by Q-PCR and western blot analyses. Chondrocytes were pre-transfected with FSTL1 overexpression plasmids then treated with SNP, and chondrocyte viability and apoptosis levels were detected by MTS and flow cytometry, respectively. Cartilage matrix gene expression was measured by Q-PCR and signal pathway-related proteins were assessed by western blot. Results: The expression of FSTL1 in OA chondrocytes was markedly up-regulated compared with normal human chondrocytes (P < 0.05). The apoptosis rate of chondrocytes in the FSTL1 overexpression groups was highly elevated in the comparison with the negative control groups (P < 0.05). Additionally, FSTL1 potentiated protein abundances of MMP1, MMP3, MMP-9, and Bax as well as reduced Coll2a1 and Aggrecan and Bcl-2 expression. Furthermore, western blot results showed that the SAPK/JNK/Caspase3 signal pathway was significantly activated and the Ac-DEVD-FMK impaired FSTL1 induced chondrocyte apoptosis. Conclusion: FSTL1 promoted SNP-induced chondrocytes apoptosis by activating the SAPK/JNK/Caspase3 signal pathway.