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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 (OA) patients from the GSE117999 dataset. The GSE48422 dataset was used to analyze the changes in the methylation level of osteoarthritis cells. Cell Counting Kit-8 (CCK-8) and flow cytometry analysis of short hairpin RNA (shRNA) silencing  CAMP  gene and 5-μM 5-Aza-2’-Deoxycytidine (AZA) treatment on the proliferation and apoptosis of Human chondrocytes osteoarthritis (HC-OA) cells. The Dichloro-dihydro-fluorescein diacetate (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 upregulated, and the level of methylation was downregulated. 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 tumor necrosis factor-α (TNF-α) expression levels in HC-OA cells, and promoted transforming growth factor beta (TGF-β) expression.  CAMP  gene methylation inhibited the proliferation of HC-OA cells and promoted their apoptosis.    Conclusion   CAMP  gene promoter methylation inhibits ROS levels and inflammation and induces chondrocyte apoptosis.

Cathelicidin antimicrobial peptide (CAMP) gene promoter methylation induces chondrocyte apoptosis