Document Detail


Experimental studies on the spatiotemporal expression of WT1 and RALDH2 in the embryonic avian heart: a model for the regulation of myocardial and valvuloseptal development by epicardially derived cells (EPDCs).
MedLine Citation:
PMID:  12086469     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Epicardially derived cells (EPDCs) delaminate from the primitive epicardium through an epithelial-to-mesenchymal transformation (EMT). After this transformation, a subpopulation of cells progressively invades myocardial and valvuloseptal tissues. The first aim of the study was to determine the tissue-specific distribution of two molecules that are thought to play a crucial function in the interaction between EPDCs and other cardiac tissues, namely the Wilms' Tumor transcription factor (WT1) and retinaldehyde-dehydrogenase2 (RALDH2). This study was performed in normal avian and in quail-to-chick chimeric embryos. It was found that EPDCs that maintain the expression of WT1 and RALDH2 initially populate the subepicardial space and subsequently invade the ventricular myocardium. As EPDCs differentiate into the smooth muscle and endothelial cell lineage of the coronary vessels, the expression of WT1 and RALDH2 becomes downregulated. This process is accompanied by the upregulation of lineage-specific markers. We also observed EPDCs that continued to express WT1 (but very little RALDH2) which did not contribute to the formation of the coronary system. A subset of these cells eventually migrates into the atrioventricular (AV) cushions, at which point they no longer express WT1. The WT1/RALDH2-negative EPDCs in the AV cushions do, however, express the smooth muscle cell marker caldesmon. The second aim of this study was to determine the impact of abnormal epicardial growth on cardiac development. Experimental delay of epicardial growth distorted normal epicardial development, reduced the number of invasive WT1/RALDH2-positive EPDCs, and provoked anomalies in the coronary vessels, the ventricular myocardium, and the AV cushions. We suggest that the proper development of ventricular myocardium is dependent on the invasion of undifferentiated, WT1-positive, retinoic acid-synthesizing EPDCs. Furthermore, we propose that an interaction between EPDCs and endocardial (derived) cells is imperative for correct development of the AV cushions.
Authors:
J M Pérez-Pomares; A Phelps; M Sedmerova; R Carmona; M González-Iriarte; R Muñoz-Chápuli; A Wessels
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Developmental biology     Volume:  247     ISSN:  0012-1606     ISO Abbreviation:  Dev. Biol.     Publication Date:  2002 Jul 
Date Detail:
Created Date:  2002-06-27     Completed Date:  2002-08-07     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0372762     Medline TA:  Dev Biol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  307-26     Citation Subset:  IM    
Copyright Information:
2002 Elsevier Science (USA).
Affiliation:
Department of Cell Biology and Anatomy, Medical University of South Carolina, Charleston, South Carolina, 29425, USA.
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MeSH Terms
Descriptor/Qualifier:
Aldehyde Oxidoreductases / biosynthesis*
Animals
Cell Differentiation
Cell Lineage
Chick Embryo
Chimera / metabolism
Gene Expression Regulation, Developmental*
Heart / embryology*
Immunohistochemistry
Keratins / metabolism
Models, Biological
Myocardium / metabolism
Pericardium / metabolism*
Phenotype
Quail
Retinal Dehydrogenase
Time Factors
WT1 Proteins / biosynthesis*
Grant Support
ID/Acronym/Agency:
1P01 HL52813-06/HL/NHLBI NIH HHS; N0-HD-2-3144/HD/NICHD NIH HHS
Chemical
Reg. No./Substance:
0/WT1 Proteins; 68238-35-7/Keratins; EC 1.2.-/Aldehyde Oxidoreductases; EC 1.2.1.36/Retinal Dehydrogenase

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