Gap junctions and biophysical regulation of bone cell differentiation

被引:144
作者
Donahue, HJ
机构
[1] Penn State Univ, Milton S Hershey Med Ctr, Dept Orthopaed & Rehabil, Musculoskeletal Res Lab,Coll Med, Hershey, PA 17033 USA
[2] Penn State Univ, Coll Med, Dept Cellular & Mol Physiol, Hershey, PA 17033 USA
关键词
connexins; mechanotransduction; osteoblasts; osteocytes; fluid flow; calcium;
D O I
10.1016/S8756-3282(00)00245-3
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Physical signals, in particular mechanical loading, are clearly important regulators of bone turnover. Indeed, the structural success of the skeleton is due in large Dart to the bone's capacity to recognize some aspect of its functional environment as a stimulus for achievement and retention of a structurally adequate morphology. However, while the skeleton's ability to respond to its mechanical environment is widely accepted, identification of a reasonable mechanism through which a mechanical "load" could be transformed to a signal relevant to the bone cell population has been elusive, Tn addition, the downstream response of bone cells to load-induced signals is unclear. In this work, we review evidence suggesting that gap junctional intercellular communication (GJIC) contributes to mechanotransduction in bone and, in so doing, contributes to the regulation of bone cell differentiation by biophysical signals. In this context, mechanotransduction is defined as transduction of a load-induced biophysical signal, such as fluid flow, substrate deformation, or electrokinetic effects, to a cell and ultimately throughout a cellular network. Thus, mechanotransduction would include interactions of extracellular signals with cellular membranes, generation of intracellular second messengers, and the propagation of these messengers, or signals they induce, through a cellular network. We propose that gap junctions contribute largely to the propagation of extracellular signals. (C) 2000 by Elsevier Science Inc. All rights reserved.
引用
收藏
页码:417 / 422
页数:6
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