Adiponectin Induces Oncostatin M Expression in Osteoblasts through the PI3K/Akt Signaling Pathway

International Journal of Molecular Sciences

Ting-Ting Lu¹  Chen-Ming Su¹  Li-Hong Wang²  Guo-Hong Xu²  Chih-Hsin Tang³  Chin-Jung Hsu⁴  Wei-Lin Lee⁵ 

[1] Department of Biomedical Sciences Laboratory, Affiliated Dongyang Hospital of Wenzhou Medical University, Dongyang 322100, China;Department of Orthopedics, Dongyang Peoples’ Hospital, Dongyang 322100, China;Graduate Institute of Basic Medical Science, China Medical University, Taichung 40402, Taiwan;School of Chinese Medicine, China Medical University, Taichung 40402, Taiwan;School of Pharmacy, China Medical University, Taichung 40402, Taiwan;

关键词: rheumatoid arthritis;    adiponectin;    oncostatin M;    osteoblasts;   

DOI  :  10.3390/ijms17010029

来源: DOAJ

【 摘 要 】

Rheumatoid arthritis (RA), a common autoimmune disorder, is associated with a chronic inflammatory response and unbalanced bone metabolism within the articular microenvironment. Adiponectin, an adipokine secreted by adipocytes, is involved in multiple functions, including lipid metabolism and pro-inflammatory activity. However, the mechanism of adiponectin performance within arthritic inflammation remains unclear. In this study, we observed the effect of adiponectin on the expression of oncostatin M (OSM), a pro-inflammatory cytokine, in human osteoblastic cells. Pretreatment of cells with inhibitors of phosphatidylinositol 3-kinase (PI3K), Akt, and nuclear factor (NF)-κB reduced the adiponectin-induced OSM expression in osteoblasts. Stimulation of the cells with adiponectin increased phosphorylation of PI3K, Akt, and p65. Adiponectin treatment of osteoblasts increased OSM-luciferase activity and p65 binding to NF-κB on the OSM promoter. Our results indicate that adiponectin increased OSM expression via the PI3K, Akt, and NF-κB signaling pathways in osteoblastic cells, suggesting that adiponectin is a novel target for arthritis treatment.

【 授权许可】

Unknown