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Int. J. Mol. Sci. 2014, 15(9), 15778-15790; doi:10.3390/ijms150915778

Leptin Induces Oncostatin M Production in Osteoblasts by Downregulating miR-93 through the Akt Signaling Pathway

1
Department of Orthopedic Surgery, Taichung Hospital, Department of Health Executive Yuan, Taichung 403, Taiwan
2
Department of Nursing, National Taichung University of Science and Technology, Taichung 403, Taiwan
3
School of Chinese Medicine, College of Chinese Medicine, China Medical University, Taichung 404, Taiwan
4
Graduate Institute of Biotechnology, National Chung Hsing University, Taichung 402, Taiwan
5
Department of Medicine and Graduate Institute of Clinical Medical Science, China Medical University, Taichung 404, Taiwan
6
Department of Orthopedic Surgery, China Medical University Hospital, Taichung 404, Taiwan
7
Department of Biotechnology, College of Health Science, Asia University, Taichung 500, Taiwan
8
Department of Orthopedic Surgery, Chang-Hua Hospital, Department of Health Executive Yuan, Changhua Country 500, Taiwan
9
Graduate Institute of Basic Medical Science, China Medical University, Taichung 404, Taiwan
10
Department of Pharmacology, School of Medicine, China Medical University, Taichung 404, Taiwan
These authors contributed equally to this work.
*
Author to whom correspondence should be addressed.
Received: 4 August 2014 / Revised: 20 August 2014 / Accepted: 3 September 2014 / Published: 5 September 2014
(This article belongs to the Section Biochemistry, Molecular and Cellular Biology)
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Abstract

Inflammatory response and articular destruction are common symptoms of osteoarthritis (OA) and rheumatoid arthritis (RA). Leptin, an adipocyte-secreted hormone that centrally regulates weight control, may exert proinflammatory effects in the joint, depending on the immune response. Yet, the mechanism of leptin interacting with the arthritic inflammatory response is unclear. This study finds that leptin increased expression of oncostatin M (OSM) in human osteoblasts in a concentration- and time-dependent manner. In addition, OBRl, but not OBRs receptor antisense oligonucleotide, abolished the leptin-mediated increase of OSM expression. On the other hand, leptin inhibited miR-93 expression; an miR-93 mimic reversed leptin-increased OSM expression. Stimulation of osteoblasts with leptin promoted Akt phosphorylation, while pretreatment of cells with Akt inhibitor or siRNA reversed leptin-inhibited miR-93 expression. Our results showed that leptin heightened OSM expression by downregulating miR-93 through the Akt signaling pathway in osteoblasts, suggesting leptin as a novel target in arthritis treatment. View Full-Text
Keywords: leptin; oncostatin M; OBRl; arthritis; miR-93 leptin; oncostatin M; OBRl; arthritis; miR-93
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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MDPI and ACS Style

Yang, W.-H.; Tsai, C.-H.; Fong, Y.-C.; Huang, Y.-L.; Wang, S.-J.; Chang, Y.-S.; Tang, C.-H. Leptin Induces Oncostatin M Production in Osteoblasts by Downregulating miR-93 through the Akt Signaling Pathway. Int. J. Mol. Sci. 2014, 15, 15778-15790.

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