Cardiovascular Research 2001 49(2):417-429; doi:10.1016/S0008-6363(00)00252-2
© 2001 by European Society of Cardiology
Copyright © 2000, European Society of Cardiology
Molecular characterization of the ventricular conduction system in the developing mouse heart: topographical correlation in normal and congenitally malformed hearts
aDepartment of Experimental Biology, Faculty of Experimental and Health Sciences, University of Jaén, Paraje Las Lagunillas s/n, 23071 Jaén, Spain
bDepartment of Anatomy and Cell Biology, University of Cantabria, Santander, Spain
* Corresponding author. Tel.: +31-20-566-4926; fax: +31-20-697-6177 d.franco{at}ujaen.es
Objectives: Within the adult heart, it is convention to distinguish the conduction system and working (atrial and ventricular) myocardium. The adult conduction system (CS) comprises the sinoatrial (SAN), and atrioventricular (AVN) nodes, the atrioventricular bundle (AVB), the bundle branches and the peripheral Purkinje fibers, each of which display distinct functional properties and distinct profile of gene expression. Characterization of the mouse cardiac conduction system during development is rudimentary at present, even though genetically-modified mice are an increasing source of information regarding cardiac function and embryonic heart development. Methods: We have performed a detailed study of the pattern of expression of myosin heavy chain (MHC), myosin light chain (MLC), troponin I (TnI) isoforms, connexin 43 (Cx43), desmin and alpha-smooth muscle actin (
-SMA), in the ventricular conduction system of normal and congenitally malformed mouse hearts (iv background) from embryonic day 14.5 to 19.5. Results: The AVN is characterized by co-expression of MHC and MLC isoforms and no detectable expression of Cx43, desmin or -SMA. The AVB expresses βMHC and MLC2v, but no MHC, MLC2a, Cx43, desmin or -SMA. The right and left bundle branches display enhanced expression of desmin and -SMA but no Cx43. The normal expression profile is maintained in congenitally malformed hearts such as double-outlet right ventricle and common atrioventricular canal. Three-dimensional reconstruction of the conduction system shows normal arrangement of the bundle branches in congenitally malformed hearts, but abnormal location and/or extension of the AVN. Conclusions: Molecular characterization allows to follow the development of the CS in both, normal and malformed mouse hearts. Normal phenotypic expression of the CS is independent of heart situs but shows minor modifications in the presence of heart malformations. It is concluded that the AVN derives from the atrioventricular canal myocardium, the bundle of His from the ventricular myocardium, and the bundle branches from the ventricular trabeculations. Our results do not provide evidence to support an extra-cardiac origin of the ventricular CS.
KEYWORDS Conduction system; Congenital defects; Gene expression
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Cardiovasc Res 2001 50: 613.
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