Basic & Clinical Medicine ›› 2015, Vol. 35 ›› Issue (8): 1089-1093.

Previous Articles     Next Articles

IL-1β induced endoplasmic reticulum stress increases human chondrocyte apoptosis and the mechanism

  

  • Received:2014-11-17 Revised:2015-03-26 Online:2015-08-05 Published:2015-07-15

Abstract: Objective To analysis the effects of inflammation factors (IL-1β, TNF-α) on endoplasmic reticulum stress (ERS) and the association with osteoarticular chondrocyte apoptosis. Methods Osteoarticular cartilage tissues were collected from normal and patients with OA (20 cases for each group). RT-PCR were performed to measure the mRNA level of IL-1β, TNF-α, GRP78 and CHOP in cartilaginous tissues. Western blot was used to evaluate the expression of GRP78, CHOP, ATF4 and caspase-3 in chondrocytes. The apoptosis of chondrocyte was analyzed by TUNEL. Results Compared with control, mRNA levels of IL-1β, TNF-α, GRP78 and CHOP in OA were significantly higher (P<0.01), while the high expression of IL-1β was positively correlated to GRP78 and CHOP (P<0.05). In vitro, GRP78, CHOP, ATF4 expression and chondrocyte apoptosis significantly increased in response to the treatment of IL-1β (2 ng/L) (P<0.01). In addition, the expression of GRP78, caspase-3 and chondrocyte apoptosis were significantly higher after incubation with TNF-α (P<0.01). Conclusion 2 ng/L and higher dosage of IL-1β triggered ATF4-CHOP-mediated ERS to induce chondrocyte apoptosis.

Key words: Osteoarthritis, IL-1β, CHOP, ER stress, cell apoptosis