Connexins and junctional channels. Roles in the spreading of cardiac electrical excitation and heart development

• Published in: Pathologie biologie (Paris) 2008-07, Vol.56 (5), p.334-341
• Main Authors: Hervé, J-C, Derangeon, M, Théveniau-Ruissy, M, Miquerol, L, Sarrouilhe, D, Gros, D
• Format: Article
• Language: fre
• Subjects: Animals; Cell Communication - physiology; Connexins - deficiency; Connexins - genetics; Connexins - physiology; Fetal Heart - growth & development; Fetal Heart - physiology; Gap Junction alpha-5 Protein; Gap Junctions - physiology; Heart - embryology; Heart Conduction System - physiology; Mice; Mice, Knockout; Mice, Transgenic; Myocytes, Cardiac - physiology; Myocytes, Cardiac - ultrastructure
• ISSN: 0369-8114
• DOI: 10.1016/j.patbio.2008.05.009

The electrical activity in heart is generated in the sinoatrial node and then propagates to the atrial and ventricular tissues. The junctional channels that couple the cardiomyocytes are responsible for this propagation process. These channels are dodecamers of transmembrane proteins of the connexin (Cx) family. Four Cxs - Cx30.2, -40, -43 and -45--have been demonstrated to be synthesized in the cardiomyocytes. In addition, each of these Cxs has a unique expression pattern in the myocardium. A fruitful approach of the role of these Cxs in the cardiac functions came with the development of transgenic mouse models. It has been shown that Cx43 was mainly involved in influx propagation in the ventricles and that inactivation in the cardiomyocytes of the gene of this Cx predisposed to development of cardiac abnormalities. Cx40 very significantly contributes to the propagation of electrical activity in the atria and the conduction system. Cx45 is essential to coordinate the synchronization of contractile activities of embryonic cardiomyocytes and for the normal progress of cardiogenesis. Finally, Cx30.2 contributes to the slowing of propagation of excitation in the atrioventricular node. These observations enable to better understand the relationships between alteration in Cx expression or gap junction remodelling and arrhythmias in the human heart.