G Protein-Coupled Receptors and Adipogenesis: A Focus on Adenosine Receptors

被引:30
作者
Eisenstein, Anna [1 ,2 ]
Ravid, Katya [1 ,2 ,3 ,4 ]
机构
[1] Boston Univ, Sch Med, Dept Med, Boston, MA 02118 USA
[2] Boston Univ, Sch Med, Whitaker Cardiovasc Inst, Boston, MA 02118 USA
[3] Boston Univ, Sch Med, Dept Biochem, Boston, MA 02118 USA
[4] Boston Univ, Sch Med, Evans Ctr Interdisciplinary Biomed Res, Boston, MA 02118 USA
基金
美国国家卫生研究院;
关键词
ENHANCER-BINDING-PROTEIN; MESENCHYMAL STEM-CELLS; INHIBITS ADIPOCYTE DIFFERENTIATION; ADIPOSE-TISSUE EXPANDABILITY; PPAR-GAMMA; GENE-EXPRESSION; CALCIUM OSCILLATIONS; ALPHA-SUBUNIT; 3T3-L1; CELLS; C/EBP-ALPHA;
D O I
10.1002/jcp.24473
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
G-protein coupled receptors (GPCRs) are a large family of proteins that coordinate extracellular signals to produce physiologic outcomes. Adenosine receptors (AR) are one class of GPCRs that have been shown to regulate functions as diverse as inflammation, blood flow, and cellular differentiation. Adenosine signals through four GPCRs that either inhibit (A1AR and A3AR) or activate (A2aAR and A2bAR) adenylyl cyclase. This review will focus on the role of GPCRs, and in particular, adenosine receptors, in adipogenesis. Preadipocytes differentiate to mature adipocytes as the adipose tissue expands to compensate for the consumption of excess nutrients. These newly generated adipocytes contribute to maintaining metabolic homeostasis. Understanding the key drivers of this differentiation process can aid the development of therapeutics to combat the growing obesity epidemic and associated metabolic consequences. Although much literature has covered the transcriptional events that culminate in the formation of an adipocyte, less focus has been on receptor-mediated extracellular signals that direct this process. This review will highlight GPCRs and their downstream messengers as significant players controlling adipocyte differentiation. J. Cell. Physiol. 229: 414-421, 2014. (c) 2013 Wiley Periodicals, Inc.
引用
收藏
页码:414 / 421
页数:8
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