Interleukin-35 Regulates Angiogenesis Through P38 Mitogen-Activated Protein Kinase Signaling Pathway In Interleukin-1 Beta-Stimulated Sw1353 Cells And Cartilage Bioinformatics Analysis

We aimed to investigate the effects of interleukin (IL)-35 on proangiogenic factors in IL-1 beta-pretreated chondrocyte-like SW1353 cells and screen-related genes that participated in osteoarthritis (OA) cartilage with IL-35, proangiogenic factors, and P38 mitogen-activated protein kinase (MAPK) signaling pathway. Different concentrations of IL-35 incubated with IL-1 beta stimulated SW1353 cells with or without SB203580 (inhibitor of P38 MAPK). Proangiogenic molecule expression was assessed by real-time polymerase chain reaction and enzyme-linked immunosorbent assay. Microarray datasets were downloaded from the Gene Expression Omnibus database of OA cartilage. Protein-protein interaction of genes was visualized by Search Tool for the Retrieval Interacting Genes and Cytoscape. Database for Annotation, Visualization, and Integrated Discovery was used to screen biological processes and pathways. IL-35 inhibited mRNA expression of proangiogenic factors in IL-1 beta-stimulated SW1353 cells through the P38 MAPK signaling pathway. IL-35 inhibited angiopoietin-2 secretion. We found that 8 related genes, 18 biological processes, and 6 pathways may associate with IL-35, P38 MAPK signaling pathway, and cartilage angiogenesis. IL-35 regulated the expression of proangiogenic factors through P38 MAPK signaling pathway in IL-1 beta-stimulated SW1353 cells. IL-35 and P38 MAPK pathway may participate in neovascularization of cartilage. Our findings may provide molecular mechanisms and possible genes target treatment for OA.