Oncotarget

Research Papers:

Leptin induces osteocalcin expression in ATDC5 cells through activation of the MAPK-ERK1/2 signaling pathway

Yingchao Han, Guanghui Xu, Jingjie Zhang, Meijun Yan, Xinhua Li, Bin Ma, Lili Jun, Shan-Jin Wang _ and Jun Tan

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Oncotarget. 2016; 7:64021-64029. https://doi.org/10.18632/oncotarget.11578

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Abstract

Yingchao Han1,*, Guanghui Xu2,*, Jingjie Zhang1, Meijun Yan1, Xinhua Li1, Bin Ma1, Lili Jun1, Shan-Jin Wang1, Jun Tan1

1Department of Spine Surgery, Shanghai East Hospital, Tongji University, School of Medicine, Shanghai, 200120, China

2Department of Orthopedics, Shanghai Zhabei District Central hospital, Zhonghuaxin Road Zhabei District, Shanghai, 200070, China

*These authors have contributed equally to this work

Correspondence to:

Shan-Jin Wang, email: [email protected]

Jun Tan, email: [email protected]

Keywords: leptin, osteocalcin, ATDC5, growth plate, chondrocyte

Received: April 18, 2016    Accepted: August 11, 2016    Published: August 24, 2016

ABSTRACT

Both leptin and osteocalcin have been found to affect growth-plate cartilage development through regulation of the physiologic processes of endochondral bone formation. Leptin mediates bone development and osteocalcin secreted in the late stage of osteoblast differentiation. The relationship between leptin and osteocalcin expression in the chondrogenic cells line is still not clear. Thus, the aim of this study was to explore the effect of leptin on the expression of osteocalcin in chondrocytes. We used clonal mouse chondrogenic ATDC5 cells to investigate the relationship between leptin and osteocalcin. We found that both leptin and osteocalcin expression were dynamically expressed during ATDC5 cell differentiation from 4 to 21 days. We also found that leptin significantly upregulated osteocalcin mRNA and protein levels 24 h after leptin stimulation. However, different concentrations and exposure times of osteocalcin did not affect the levels of leptin protein. Furthermore, we confirmed that leptin augmented the phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) in a time-dependent manner but not p38 or AKT. Inhibition of pERK1/2 expression by a specific ERK1/2 inhibitor U0126 and a special small interfering RNA attenuated levels of leptin-induced osteocalcin expression, indicating that ERK1/2 mediates, in part, the effects of leptin on osteocalcin. Taken together, our results suggest that leptin regulates the expression of osteocalcin in growth plate chondrocytes via the ERK1/2 signaling pathway, while there is no effect on the phosphorylation of either p38 or AKT.


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