Linked Life Data

11934868

Source:http://linkedlifedata.com/resource/pubmed/id/11934868

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2002-4-5
pubmed:abstractText
Connexin43 knockout mice die neonatally from conotruncal heart malformation and outflow obstruction. Previous studies have indicated the involvement of neural crest perturbations in these cardiac anomalies. We provide evidence for the involvement of another extracardiac cell population, the proepicardial cells. These cells give rise to the vascular smooth muscle cells of the coronary arteries and cardiac fibroblasts in the heart. We have observed the abnormal presence of fibroblast and vascular smooth muscle cells in the infundibular pouches of the connexin43 knockout mouse heart. In addition, the connexin43 knockout mice exhibit a variety of coronary artery patterning defects previously described for neural crest-ablated chick embryos, such as anomalous origin of the coronary arteries, absent left or right coronary artery, and accessory coronary arteries. However, we show that proepicardial cells also express connexin43 gap junctions abundantly. The proepicardial cells are functionally well coupled, and this coupling is significantly reduced with the loss of connexin43 function. Further analysis revealed an elevation in the speed of cell locomotion and cell proliferation rate in the connexin43-deficient proepicardial cells. A parallel analysis of proepicardial cells in transgenic mice with dominant negative inhibition of connexin43 targeted only to neural crest cells showed none of these coupling, proliferation or migration changes. These mice exhibit outflow obstruction, but no infundibular pouches. Together these findings indicate an important role for connexin43 in coronary artery patterning, a role that probably involves the proepicardial and cardiac neural crest cells. We discuss the potential involvement of connexin43 in human cardiovascular anomalies involving the coronary arteries.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0950-1991
pubmed:author
pubmed:issnType
Print
pubmed:volume
129
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2031-42
pubmed:dateRevised
2011-11-10
pubmed:meshHeading
pubmed-meshheading:11934868-Animals, pubmed-meshheading:11934868-Biological Markers, pubmed-meshheading:11934868-Cell Differentiation, pubmed-meshheading:11934868-Cell Division, pubmed-meshheading:11934868-Cell Movement, pubmed-meshheading:11934868-Connexin 43, pubmed-meshheading:11934868-Coronary Circulation, pubmed-meshheading:11934868-Coronary Vessels, pubmed-meshheading:11934868-Gap Junctions, pubmed-meshheading:11934868-Heart, pubmed-meshheading:11934868-Mice, pubmed-meshheading:11934868-Mice, Inbred C57BL, pubmed-meshheading:11934868-Mice, Knockout, pubmed-meshheading:11934868-Microfilament Proteins, pubmed-meshheading:11934868-Muscle, Smooth, Vascular, pubmed-meshheading:11934868-Muscle Proteins, pubmed-meshheading:11934868-Myosins, pubmed-meshheading:11934868-Neovascularization, Physiologic, pubmed-meshheading:11934868-Pericardium
pubmed:year
2002
pubmed:articleTitle
An essential role for connexin43 gap junctions in mouse coronary artery development.
pubmed:affiliation
Biology Department, Goddard Laboratories, University of Pennsylvania, Philadelphia, PA, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't