Glucocorticoids Induces Apoptosis in Chondrocytes Through the Regulation of 11β-Hydroxysteroid Dehydrogenases (11β-HSDs)

Abstract

Chondrocytes maintain the cartilaginous matrix and play an important role in endochondral ossification and cartilage repair. The regulation of chondrocyte proliferation and apoptosis is important in the pathology of cartilage and bone damage disorders. Recent studies have shown that glucocorticoids may induce apoptosis in chondrocytes. 11β-hydroxysteroid dehydrogenases (11β-HSDs) are microsomal enzymes that catalyze the interconversion of active 11-hydroxy-glucocorticoids and the inert 11-keto forms. We conducted an in vitro study to investigate the role of 11β-HSDs in apoptosis in femoral head chondrocytes. Our data showed that dexamethasone could induce chondrocyte apoptosis and cell viability reduction. Using Western blotting and real-time quantitative PCR, we observed that increased concentrations of dexamethasone increased the expression of 11β-HSD-1 and decreased the expression of 11β-HSD-2. Based on these results, we conclude that 11β-HSDs may be important for the regulation of glucocorticoid-induced apoptosis in chondrocytes. The present study demonstrates that glucocorticoids are able to induce both apoptosis in chondrocytes and a reduction in cell viability. Furthermore, 11β-HSDs may be important for the regulation of glucocorticoid-induced apoptosis in chondrocytes.