Basic & Clinical Medicine ›› 2018, Vol. 38 ›› Issue (9): 1309-1314.

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Silencing of FSTL1 silence reduces tunicamycin-induced endoplasmic reticulum stress and apoptosis in chondrocytes


  • Received:2017-05-22 Revised:2017-10-12 Online:2018-09-05 Published:2018-09-10

Abstract: Objective To investigate the effects of specific silencing of follistatin-like protein 1 (FSTL1) on tunicamycin-induced endoplasmic reticulum stress and apoptosis in chondrocytes. Methods Rabbit knee articular cartilage was obtained. Chondrocytes were harvested and cultured. The cells were divided into control group, tunicamycin group, tunicamycin+siRNA-FSTL1 group and tunicamycin+siRNA-NC group. The cell proliferation was detected by MTT assay. Cell apoptosis was detected by flow cytometry. The expressions of FSTL1, Bcl-2 and Bax genes were detected by real-time fluorescence quantitative polymerase chain reaction. The expressions of PERK, p-PERK, GRP78, ATF4, CHOP, Cal, eIF2α and p-eIF2α proteins were detected by Western blot. Results Compared with the tunicamycin group and tunicamycin+siRNA-NC group, the cell proliferation abilities in tunicamycin+siRNA-FSTL1 group were significantly increased (P<0.05), the apoptotic rate was decreased (P<0.05), the relative expression levels of FSTL1 and Bax mRNA were decreased, while the relative expression level of Bcl-2 mRNA was increased (P<0.05), the relative expression levels of PERK and eIF2α proteins were increased, while the relative expression levels of p-PERK, GRP78, ATF4, CHOP, Cal and p-eIF2α proteins were decreased (P<0.05). Conclusions Specific silencing of FSTL1 gene expression in chondrocytes could effectively reduce ERS and apoptosis. The mechanism might be related to inhibition of PERK signal pathway.

Key words: Keywords: chondrocytes, follistatin-like protein 1, small RNA interference, endoplasmic reticulum stress, apoptosis