TNF-α activates RELA expression via TNFRSF1B to upregulate OPA1 expression and inhibit chondrogenic differentiation of human adipose stem cells

Tumour necrosis factor-alpha (TNF-α), one of the pro-inflammatory cytokines mediating the local inflammatory process in joints, has an inhibitory effect on cartilage formation and has a detrimental effect on stem cell-based cartilage regeneration for the treatment of osteoarthritis (OA). However, the mechanisms behind this inhibitory effect are still poorly understood. Mitochondria are important organelles that play a vital role in maintaining the structure and function of the cell. Our study aimed to investigate the role and mechanisms of regulation of mitochondrial fusion and fission in the chondrogenic differentiation of human adipose stem cells (hADSCs) in the absence and presence of TNF-α. Affmetrix PrimeViewTM chips for gene expression profiling. The results of the previous experiments were summarized by observing that the expression levels of OPA1, DNM1L, mitochondrial morphology, and ROS levels were significantly different in the Chondro-TNF-α group compared to the Chondro group at 7 days of chondrogenic differentiation. Therefore, we prepared hADSCs from the Chondro group and Chondro-TNF-α group into cartilage differentiation at 7 days as well as hADSCs from the control group (differentiation 0 d) for gene expression profiling.