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Int. J. Mol. Sci. 2016, 17(1), 29; doi:10.3390/ijms17010029

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

1
Department of Biomedical Sciences Laboratory, Affiliated Dongyang Hospital of Wenzhou Medical University, Dongyang 322100, China
2
School of Pharmacy, China Medical University, Taichung 40402, Taiwan
3
School of Chinese Medicine, China Medical University, Taichung 40402, Taiwan
4
Department of Orthopedic Surgery, China Medical University Hospital, Taichung 40402, Taiwan
5
Department of Orthopedics, Dongyang Peoples’ Hospital, Dongyang 322100, China
6
Graduate Institute of Basic Medical Science, China Medical University, Taichung 40402, Taiwan
7
Department of Pharmacology, School of Medicine, China Medical University, Taichung 40402, Taiwan
8
Department of Biotechnology, College of Health Science, Asia University, Taichung 41354, Taiwan
*
Author to whom correspondence should be addressed.
Academic Editor: Sanjay K. Srivastava
Received: 10 November 2015 / Revised: 16 December 2015 / Accepted: 22 December 2015 / Published: 25 December 2015
(This article belongs to the Section Biochemistry, Molecular and Cellular Biology)
View Full-Text   |   Download PDF [1243 KB, uploaded 25 December 2015]   |  

Abstract

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. View Full-Text
Keywords: rheumatoid arthritis; adiponectin; oncostatin M; osteoblasts rheumatoid arthritis; adiponectin; oncostatin M; osteoblasts
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MDPI and ACS Style

Su, C.-M.; Lee, W.-L.; Hsu, C.-J.; Lu, T.-T.; Wang, L.-H.; Xu, G.-H.; Tang, C.-H. Adiponectin Induces Oncostatin M Expression in Osteoblasts through the PI3K/Akt Signaling Pathway. Int. J. Mol. Sci. 2016, 17, 29.

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