Adiponectin On Synovial Cells And PSCs Role

Objective:To analyze the expression levels of adiponectin receptors in synovial fibroblasts, and evaluate the molecular mechanismsroles in adiponectin-induced prostaglandin E2(PGE2) production; isolate mesenchymal stem cells (MSCs) from articular cartilage of later stages of osteoarthritis using a new stem cell marker, and verify the characteristics of these cells; then investigate the role of adiponectin on chondrogenic differentiation of chondrogenic progenitor cells.Methods:Compared the expression of adiponectin receptors(Adipo R) in rheumatoid arthritis synovial fibroblasts (RASF) and osteoarthritis synovial fibroblasts (OASF) from the gene and protein level, evaluated the role of adiponectin receptors in adiponectin-induced prostaglandin E2(PGE2) production, and made a preliminary study on its mechanism. Isolated MSCs from articular cartilage of later stages of osteoarthritis using a new stem cell marker CD146, and compared the differentiation capacity with the MSCs from adipose tissue. Finally, chondrogenic induction of the chondrogenic progenitor cells with adiponectin intervention, observated the influence of adiponectin on its chondrogenic differentiation.Results:AdipoRl and AdipoR2mRNA and protein were expressed by both RASF and OASF. Compared with OASF, RASF exhibited higher levels of AdipoRl, but there was no significant difference for AdipoR2. Adiponectin induced the production of PGE2by synovial fibroblasts in a concentration-dependent manner, and this was more obvious in RASF.RNA interference showed that the difference may be mediated by the diverse distribution of AdipoRl. When OASF stimulated with adiponectin, it can be found that PGE2synthesis relate genes COX-2, mPGES-1mRNA expression were raised and the adiponectin-induced PGE2production was efficiently relieved by the NSAID and COX-2-selective inhibitor. CD146+cells from articular cartilage expressed special stem cell surface markers, exhibited ability of clonogenicity, muti-differentiation into adipocytes, osteoblasts and chondrocytes, and were superior to adipose tissue derived MSCs and unsorted chondrocytes in terms of chondrogenesis,but the adipogenesis and osteogenesis were less than MSCs from adipose tissue. In chondrogenic induction process, it will weaken the ability of chondrogenic differentiation of chondrogenic progenitor cells when applied adiponectin intervention.Conclution:Adiponectin induced the production of PGE2by synovial fibroblasts, and AdipoRl plays a more important role in the inflammatory response.The chondrogenic progenitor cells were exist in the degeneration of articular cartilage,and adiponectin can inhibit chondrogenic potential of chondrogenic progenitor cells. Adiponectin not only promote the development of OA on mature cellular levels, but also interfere with stem cells participation in tissue repair.