KLF11 protects chondrocytes via inhibiting p38 MAPK signaling pathway.

Abstract

The purpose of this study was to explore the effects of Kruppel like factors 11 (KLF11) on oxidative stress, apoptosis, and endoplasmic reticulum stress (ERS) in osteoarthritis (OA) and its mechanism. Human articular cartilage tissue was used to study the correlation between KLF11 and OA. Furthermore, human chondrocytes were used to explore the effects of KLF11 on oxidative stress, apoptosis, and ERS in chondrocytes by overexpressing KLF11 and using the OA inducer IL-1β. The p38MAPK signaling pathway agonist P79350 was used to study the effect of KLF11 on the p38 MAPK signaling pathway. Articular cartilage tissue in OA patients and IL-1β-induced chondrocytes expressed higher KLF11. Overexpression of KLF11 significantly reduced oxidative stress levels, apoptosis levels, and activity of ERS-related pathways in chondrocytes. Moreover, P79350 attenuated the protective effect of KLF11 on chondrocytes by activating the p38MAPK signaling pathway. KLF11 protects against OA by inhibiting oxidative stress, apoptosis, and ERS in chondrocytes by inhibiting p38MAPK signaling pathway.