Genetic deletion of GIT2 prolongs functional recovery and suppresses chondrocyte differentiation in rats with rheumatoid arthritis

Abstract

The current study was conducted for investigating the mechanism by which GIT2 gene deletion affects the functional recovery and chondrocyte differentiation in rats with rheumatoid arthritis (RA). Thirty-two rats were randomly divided into normal, model, GIT2 gene knockout (GIT2-KO), and model + GIT2-KO groups. Hematoxylin-eosin (HE) staining was performed for the observation of synovial tissues. Immunohistochemistry examinations were conducted to determine type II collagen expression as well as identify chondrocyte differentiation. qRT-PCR and Western blotting techniques were adopted in order to expressions of interleukin-1β (1L-1β), tumor necrosis factor-α (TNF-α), Aggrecan, and Sry-related HMG box 9 (Sox9). A tape measure and Vernier caliper were used to measure the degree of swelling. Compared with synovial tissues in the model group, those in the model + GIT2-KO group, were thicker and comprised of a mass of inflammatory cells (P < 0.05). Compared with the model group, the type II collagen expressions of the cartilage tissues of the rats decreased in the model + GIT2-KO group (P < 0.05). In terms of the degree of swelling in cartilage tissues, the model group displayed a lesser degree of swelling than in that of the model + GIT2-KO group (P < 0.05). When compared with the model + GIT2-KO group, the mRNA expressions of 1L-1β, TNF-α, Aggrecan, Sox9 and the relevant protein expressions were lower in the model group (all P < 0.05). GIT2 gene deletion might weaken chondrocyte differentiation in rats with RA, as a result acting to ultimately prolong the functional recovery of RA.

Keywords: GIT2; cartilage tissues; chondrocyte differentiation; functional recovery; gene deletion; rheumatoid arthritis.