Abstract
Osteoarthritis (OA) is a kind of arthritis that impairs movement and causes joint discomfort. Recent research has demonstrated a connection between cellular senescence and the degenerative processes of OA chondrocytes. In yeast and human cells, protein tyrosine phosphatase 1B (PTP1B) knockdown prolongs longevity; however, the function of PTP1B in chondrocyte senescence has not been investigated. The goal of the current investigation was to evaluate PTP1B's contribution to human OA chondrocyte senescence. The function of PTP1B and cellular senescence in the onset of OA was investigated and confirmed by using a combination of bioinformatics techniques, clinical samples, and in vitro experimental procedures. The RNA sequencing data pertinent to the OA were obtained using the Gene Expression Omnibus database. Function enrichment analysis, protein-protein correlation analysis, the construction of the correlation regulatory network, and an investigation into possible connections between PTP1B and cellular senescence in OA were all carried out using various bioinformatic techniques. Compared with healthy cartilage, PTP1B expression was increased in OA cartilage. According to a Pearson correlation study, cellular senescence-related genes, including MAP2K1 and ABL1, were highly correlated with PTP1B expression levels in senescent chondrocytes. Furthermore, in vitro tests confirmed that PTP1B knockdown slowed cartilage degradation and prevented chondrocyte senescence in OA. In conclusion, we showed that PTP1B knockdown prevented the senescence of chondrocytes and prevented cartilage degradation in OA. These findings offer a fresh perspective on the pathophysiology of OA, opening up new avenues for OA clinical diagnosis and targeted treatment.