MAP kinase phosphatase 3 inhibits brown adipocyte differentiation via regulation of Erk phosphorylation

被引:9
作者
Kim, Won Kon [1 ,2 ]
Oh, Kyoung-Jin [1 ]
Choi, Hye-Ryung [1 ]
Park, Anna [1 ]
Han, Baek Soo [1 ,2 ]
Chi, Seung-Wook [1 ]
Kim, Seung Jun [1 ]
Bae, Kwang-Hee [1 ,2 ]
Lee, Sang Chul [1 ,2 ]
机构
[1] KRIBB, Funct Genom Res Ctr, Taejon 305806, South Korea
[2] Univ Sci & Technol Korea, Dept Funct Genom, Taejon 305806, South Korea
基金
新加坡国家研究基金会;
关键词
Brown adipogenesis; ERK; MKP3; Obesity; MESENCHYMAL STEM-CELLS; TYROSINE-PHOSPHATASE; ADIPOSE-TISSUE; ADIPOGENIC DIFFERENTIATION; FAT; ACTIVATION; TRANSCRIPTION; EXPRESSION; PATHWAY;
D O I
10.1016/j.mce.2015.08.023
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Brown fat has been highlight as a new therapeutic target for treatment of obesity and diabetes. However, molecular mechanism underlying brown adipogenesis are not fully understood. Here, we identified that MAP kinase phosphatase 3 (MKP3) has a novel role as regulator of brown adipocyte differentiation. The expression of MKP3 was significantly decreased during the early stage(s) of brown adipocyte differentiation in HIB-1B cells and primary cells. Ectopic expression of MKP3 led to reduced brown adipocyte differentiation, whereas depletion of MKP3 significantly enhanced the differentiation of primary brown preadipocytes. Consistently, we found an increased brown adipocyte differentiation in MKP3-null MEF cells. These inhibitory effects of MKP3 could be resulted via the temporal regulation of Erk activation. In recent, it was reported that MKP3 deficient mice are resistant to diet-induced obesity, and display enhanced energy expenditure. Taken together, we suggest that MKP3 could be an important factor in the regulation of brown adipocyte differentiation. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:70 / 76
页数:7
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