Reg3β promotes chondrocyte proliferation and ECM metabolism during acetabular roof remodeling in a rat model of DDH‑induced residual dysplasia.

Abstract

Residual acetabular dysplasia (RAD) is a common complication after the successful management of developmental dysplasia of the hip (DDH). RAD remodeling is important for predicting the outcome of the affected hip, and optimal treatment can be chosen accordingly. Regenerating islet‑derived protein 3‑β (Reg3β), a multifaceted cytokine, is a prognostic marker for inflammation and cardiac disease. Nevertheless, the roles of Reg3β in RAD remain unclear. Consequently, the aim of the present study was to assess the role of Reg3β in RAD and explore its related functions in chondrocytes in vitro. First, remodeling of the affected hip after fixation removal was observed in a neonatal rat DDH model, which simulated the process of RAD. Reg3β expression in RAD was upregulated at weeks 1, 2 and 4, as determined by western blot analysis. The serum concentration of Reg3β was greater than that of normal rats at 2 weeks and returned to normal levels at 4 weeks. Subsequently, it was found that Reg3β promoted cell proliferation and extracellular matrix (ECM) metabolism via the Jak2/Stat3/Socs3 signaling pathway through gene knockdown and addition of recombinant Reg3β protein. These findings suggest that Reg3β is a novel potent prognostic biomarker for the remodeling of RAD via regulation of chondrocyte proliferation and metabolism of the ECM.