| Molecular characterization of the ventricular conduction system in the developing mouse heart: topographical correlation in normal and congenitally malformed hearts. | |
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MedLine Citation:
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PMID: 11164852 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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 (alpha-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 alpha-SMA. The AVB expresses betaMHC and MLC2v, but no alphaMHC, MLC2a, Cx43, desmin or alpha-SMA. The right and left bundle branches display enhanced expression of desmin and alpha-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. |
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Authors:
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D Franco; J M Icardo |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Cardiovascular research Volume: 49 ISSN: 0008-6363 ISO Abbreviation: Cardiovasc. Res. Publication Date: 2001 Feb |
Date Detail:
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Created Date: 2001-02-22 Completed Date: 2001-04-12 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 0077427 Medline TA: Cardiovasc Res Country: Netherlands |
Other Details:
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Languages: eng Pagination: 417-29 Citation Subset: IM |
Affiliation:
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Department of Experimental Biology, Faculty of Experimental and Health Sciences, University of Jaén, Paraje Las Lagunillas s/n, 23071, Jaén, Spain. dfranco@ujaen.es |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Actins
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genetics,
metabolism Animals Atrioventricular Node / embryology, metabolism Bundle of His / embryology, metabolism Connexin 43 / genetics, metabolism Desmin / genetics, metabolism Gestational Age Heart Atria / embryology, metabolism Heart Conduction System / embryology*, metabolism Heart Defects, Congenital / embryology*, metabolism Heart Ventricles / embryology, metabolism Image Processing, Computer-Assisted Immunohistochemistry In Situ Hybridization Mice Mice, Mutant Strains Myosin Heavy Chains / genetics, metabolism Myosin Light Chains / genetics, metabolism Protein Isoforms / genetics, metabolism RNA, Messenger / analysis Sinoatrial Node / embryology, metabolism Troponin I / genetics, metabolism |
| Chemical | |
Reg. No./Substance:
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0/Actins; 0/Connexin 43; 0/Desmin; 0/Myosin Heavy Chains; 0/Myosin Light Chains; 0/Protein Isoforms; 0/RNA, Messenger; 0/Troponin I |
| Comments/Corrections | |
Comment In:
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Cardiovasc Res. 2001 Jun;50(3):610-2
[PMID:
11392355
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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