Document Detail


Loss of microRNAs in neural crest leads to cardiovascular syndromes resembling human congenital heart defects.
MedLine Citation:
PMID:  20884876     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: Congenital heart defects represent the most common human birth defects. Even though the genetic cause of these syndromes has been linked to candidate genes, the underlying molecular mechanisms are still largely unknown. Disturbance of neural crest cell (NCC) migration into the derivatives of the pharyngeal arches and pouches can account for many of the developmental defects. The goal of this study was to investigate the function of microRNA (miRNA) in NCCs and the cardiovascular system.
METHODS AND RESULTS: We deleted Dicer from the NCC lineage and showed that Dicer conditional mutants exhibit severe defects in multiple craniofacial and cardiovascular structures, many of which are observed in human neuro-craniofacial-cardiac syndrome patients. We found that cranial NCCs require Dicer for their survival and that deletion of Dicer led to massive cell death and complete loss of NCC-derived craniofacial structures. In contrast, Dicer and miRNAs were not essential for the survival of cardiac NCCs. However, the migration and patterning of these cells were impaired in Dicer knockout mice, resulting in a spectrum of cardiovascular abnormalities, including type B interrupted aortic arch, double-outlet right ventricle, and ventricular septal defect. We showed that Dicer loss of function was, at least in part, mediated by miRNA-21 (miR-21) and miRNA-181a (miR-181a), which in turn repressed the protein level of Sprouty 2, an inhibitor of Erk1/2 signaling.
CONCLUSIONS: Our results uncovered a central role for Dicer and miRNAs in NCC survival, migration, and patterning in craniofacial and cardiovascular development which, when mutated, lead to congenital neuro-craniofacial-cardiac defects.
Authors:
Zhan-Peng Huang; Jian-Fu Chen; Jenna N Regan; Colin T Maguire; Ru-Hang Tang; Xiu Rong Dong; Mark W Majesky; Da-Zhi Wang
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-09-30
Journal Detail:
Title:  Arteriosclerosis, thrombosis, and vascular biology     Volume:  30     ISSN:  1524-4636     ISO Abbreviation:  Arterioscler. Thromb. Vasc. Biol.     Publication Date:  2010 Dec 
Date Detail:
Created Date:  2010-11-18     Completed Date:  2010-12-21     Revised Date:  2011-12-21    
Medline Journal Info:
Nlm Unique ID:  9505803     Medline TA:  Arterioscler Thromb Vasc Biol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2575-86     Citation Subset:  IM    
Affiliation:
Department of Cell and Developmental Biology, McAllister Heart Institute, School of Medicine, University of North Carolina, Chapel Hill, USA.
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MeSH Terms
Descriptor/Qualifier:
Abnormalities, Multiple / embryology,  genetics*,  pathology
Animals
Cell Death
Cell Differentiation
Cell Movement
Cell Survival
Craniofacial Abnormalities / embryology,  genetics*,  pathology
Embryo, Mammalian / abnormalities,  metabolism
Extracellular Signal-Regulated MAP Kinases / metabolism
Gene Expression Regulation, Developmental*
Genotype
Heart Defects, Congenital / embryology,  genetics*,  pathology
Humans
Membrane Proteins / metabolism
Mice
Mice, Knockout
MicroRNAs / metabolism*
Mitogen-Activated Protein Kinase Kinases / metabolism
Neural Crest / metabolism*,  pathology
Phenotype
Ribonuclease III / deficiency,  genetics*
Severity of Illness Index
Syndrome
Grant Support
ID/Acronym/Agency:
R01 HL085635-04/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/MIRN21 microRNA, mouse; 0/Membrane Proteins; 0/MicroRNAs; 0/Spry2 protein, mouse; 0/mirn181 microRNA, mouse; EC 2.7.11.24/Extracellular Signal-Regulated MAP Kinases; EC 2.7.12.2/Mitogen-Activated Protein Kinase Kinases; EC 3.1.26.3/Ribonuclease III

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