CAMP Gene Promoter Methylation Induces Chondrocyte Apoptosis By Inhibiting ROS Levels And Inflammatory Response
Abstract Objective: The occurrence of osteoarthritis is related to genetic and environmental factors. Among them, the change of chondrocyte gene expression pattern regulated by epigenetic modification is an important participant. This study analyzed the effect of CAMP gene methylation on the level of oxidative stress and inflammation of chondrocytes. Methods: We analyzed the changes of the transcriptome in the articular cartilage tissue of osteoarthritis patients (OA) from the GSE117999 dataset. The GSE48422 dataset was used to analyze the changes in the methylation level of osteoarthritis cells. MTT assay and flow cytometry analysis of short hairpin RNA (shRNA) silencing CAMP gene and 5μM 5-Aza-2’-Deoxycytidine (AZA) treatment on the proliferation and apoptosis of Human Chondrocytes Osteoarthritis (HC-OA) cells. The DCFH-DA assay was used to detect the level of reactive oxygen species (ROS), and the expression level of inflammatory factors was analyzed by Western Blot. Results: The expression of CAMP in cartilage tissue of OA patients was up-regulated, and the level of methylation was down-regulated. CAMP was highly expressed in osteoarthritis articular cartilage cells. Silencing CAMP inhibited the proliferation of HC-OA cells and promoted their apoptosis. CAMP gene methylation inhibited ROS levels and TNF-α expression levels in HC-OA cells, and promoted TGF-β expression. CAMP gene methylation inhibited the proliferation of HC-OA cells and promoted their apoptosis. Conclusion: CAMP gene promoter methylation induces chondrocyte apoptosis by inhibiting ROS levels and inflammation.