Effects of Selenium-mediated RUNX2 Overexpression and its Transcriptome Alterations on Chondrocyte Injury in Kashin Beck disease
Runt-related transcription factor 2 (RUNX2) is a key regulator of chondrocyte differentiation and apoptosis. To investigate the downstream molecular mechanisms of RUNX2 in chondrocyte injury, we established a RUNX2 overexpression model using lentiviral transfection in human chondrocytes. Total RNA was extracted from RUNX2-overexpressing and control chondrocytes and subjected to RNA sequencing. Differential expression analysis identified 263 upregulated and 216 downregulated genes in RUNX2-overexpressing cells compared with controls. Functional enrichment analysis revealed that these genes were predominantly involved in TNF and MAPK signaling pathways, suggesting that RUNX2 activation promotes inflammatory and apoptotic processes in chondrocytes. These results provide a comprehensive transcriptomic resource for understanding RUNX2-mediated signaling in cartilage degeneration and may contribute to elucidating the molecular pathogenesis of osteoarthropathy such as Kashin-Beck disease. Overall design: Human chondrocytes were transfected with a lentiviral vector encoding RUNX2 or an empty vector as control. Total RNA was isolated from each group (three biological replicates per condition) and subjected to high-throughput RNA sequencing for differential gene expression and pathway enrichment analysis.