Gap junctional regulation of signal transduction in bone cells

被引:64
作者
Buo, Atum M. [1 ]
Stains, Joseph P. [1 ]
机构
[1] Univ Maryland, Sch Med, Dept Orthopaed, Baltimore, MD 21201 USA
基金
美国国家卫生研究院;
关键词
Connexin43; Gap junction; Bone; Signal transduction; Runx2; Osterix; Osteoblast; Osteocyte; KINASE-C-DELTA; PARATHYROID-HORMONE; OCULODENTODIGITAL DYSPLASIA; CONNEXIN43; INTERACTS; OSTEOCYTE APOPTOSIS; OSTEOBLASTIC CELLS; MECHANICAL STRAIN; GENE-EXPRESSION; GJA1; MUTATIONS; CORTICAL BONE;
D O I
10.1016/j.febslet.2014.01.025
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
The role of gap junctions, particularly that of connexin43 (Cx43), has become an area of increasing interest in bone physiology. An abundance of studies have shown that Cx43 influences the function of osteoblasts and osteocytes, which ultimately impacts bone mass acquisition and skeletal homeostasis. However, the molecular details underlying how Cx43 regulates bone are only coming into focus and have proven to be more complex than originally thought. In this review, we focus on the diverse molecular mechanisms by which Cx43 gap junctions and hemichannels regulate cell signaling pathways, gene expression, mechanotransduction and cell survival in bone cells. This review will highlight key signaling factors that have been identified as downstream effectors of Cx43 and the impact of these pathways on distinct osteoblast and osteocyte functions. (C) 2014 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.
引用
收藏
页码:1315 / 1321
页数:7
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