Gap junctions, homeostasis, and injury
Article first published online: 8 APR 2002
Copyright © 2002 Wiley-Liss, Inc.
Journal of Cellular Physiology
Volume 191, Issue 3, pages 269–282, June 2002
How to Cite
De Maio, A., Vega, V. L. and Contreras, J. E. (2002), Gap junctions, homeostasis, and injury. J. Cell. Physiol., 191: 269–282. doi: 10.1002/jcp.10108
- Issue published online: 19 APR 2002
- Article first published online: 8 APR 2002
- Manuscript Accepted: 18 FEB 2002
- Manuscript Received: 29 JAN 2002
- NIH. Grant Numbers: GM57317, GM50878
- Robert Garrett Research Foundation
Gap junctions (Gj) play an important role in the communication between cells of many tissues. They are composed of channels that permit the passage of ions and low molecular weight metabolites between adjacent cells, without exposure to the extracellular environment. These pathways are formed by the interaction between two hemichannels on the surface of opposing cells. These hemichannels are formed by the association of six identical subunits, named connexins (Cx), which are integral membrane proteins. Cell coupling via Gj is dependent on the specific pattern of Cx gene expression. This pattern of gene expression is altered during several pathological conditions resulting in changes of cell coupling. The regulation of Cx gene expression is affected at different levels from transcription to post translational processes during injury. In addition, Gj cellular communication is regulated by gating mechanisms. The alteration of Gj communication during injury could be rationalized by two opposite theories. One hypothesis proposes that the alteration of Gj communication attenuates the spread of toxic metabolites from the injured area to healthy organ regions. The alternative proposition is that a reduction of cellular communication reduces the loss of important cellular metabolisms, such as ATP and glucose. © 2002 Wiley-Liss, Inc.