Fibrosis factor CTGF facilitates VCAM‑1‑dependent monocyte adhesion to osteoarthritis synovial fibroblasts via the FAK and JNK pathways.

Abstract

Osteoarthritis (OA) is a long‑term, degenerative joint disease that presents significant clinical challenges and imposes considerable financial burdens. Fibrosis is closely intertwined with the pathogenesis of various degenerative diseases, including OA. Using data from the GDS5401 dataset, the present study determined that expression levels of the fibrosis factor connective tissue growth factor (CTGF) were significantly higher in OA patients than in normal individuals. The present study also identified CTGF elevated expression levels in both OA patients compared with healthy controls and in rats with anterior cruciate ligament transection‑induced OA versus controls. Stimulating OA synovial fibroblasts (OASFs) with CTGF was shown to promote vascular cell adhesion molecule‑1 (VCAM‑1) production, thereby facilitating monocyte adhesion to OASFs. Analysis of a large dataset revealed that monocytes are the only mononuclear cells with significantly elevated levels in OA patients. It also appeared that CTGF‑induced VCAM‑1 production and monocyte adhesion were mediated via the focal adhesion kinase and JNK pathways. These findings suggest that CTGF contributes to OA progression by enhancing monocyte adhesion to the synovial membrane.