Linked Life Data

12485443

Source:http://linkedlifedata.com/resource/pubmed/id/12485443

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2002-12-17
pubmed:abstractText
We conducted this study to analyze endothelial cell function within intact thoracic aorta of the systemic sclerosis murine model, the heterozygous tight-skin mice 1: (i) assessing the distribution and activation intensity of endothelial cells, responsive to endothelium-dependent vasodilators (acetylcholine, adenosine triphosphate, bradykinin, and substance P) and Iloprost, using laser line confocal microscopy in combination with two Ca2+ fluorescent dyes; (ii) evaluating en-dothelium-dependent vasodilator- and Iloprostinduced relaxation, using isometric tension measurement; and (iii) investigating the role of nitric oxide in mediating relaxation to acetylcholine and adenosine triphosphate. The number of activated endothelial cells was significantly lower in heterozygous tight-skin mice 1, compared with controls, for adenosine triphosphate and Iloprost. Maximal increase of Ca2+ fluorescence intensity ratio in activated endothelial cells was decreased for adenosine triphosphate, bradykinin, and Iloprost, in heterozygous tight-skin mice 1. Adenosine triphosphate- and Iloprost-mediated aortic relaxation was further impaired in heterozygous tight-skin mice 1. Finally, aortic relaxation to acetylcholine and adenosine triphosphate was markedly decreased by nitric oxide synthase inhibitor in heterozygous tight-skin mice 1. This study suggests that endothelial cell receptors for endothelium-dependent vasodilators and Iloprost may not be homogeneously distributed or continuously expressed in thoracic aorta of heterozygous tight-skin mice 1, resulting in endothelium-dependent vasodilatation dysfunction. Moreover, because endothelium-dependent relaxation was highly dependent on nitric oxide release in heterozygous tight-skin mice 1, endothelium-dependent relaxation may differ from that of controls by increased production of nitric oxide. In turn, in heterozygous tight-skin mice 1, the resulting elevated nitric oxide levels may contribute to nitric oxide-mediated free radical endothelial cytotoxicity, although endothelium impairment may be related to other factors, particularly: Fbn-1 gene mutation and transforming growth factor-beta.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0022-202X
pubmed:author
pubmed:issnType
Print
pubmed:volume
119
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1379-87
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:12485443-Acetylcholine, pubmed-meshheading:12485443-Adenosine Triphosphate, pubmed-meshheading:12485443-Animals, pubmed-meshheading:12485443-Aorta, Thoracic, pubmed-meshheading:12485443-Bradykinin, pubmed-meshheading:12485443-Calcium, pubmed-meshheading:12485443-Disease Models, Animal, pubmed-meshheading:12485443-Endothelium, Vascular, pubmed-meshheading:12485443-Iloprost, pubmed-meshheading:12485443-Isometric Contraction, pubmed-meshheading:12485443-Mice, pubmed-meshheading:12485443-Mice, Inbred C57BL, pubmed-meshheading:12485443-Mice, Mutant Strains, pubmed-meshheading:12485443-Microscopy, Confocal, pubmed-meshheading:12485443-Nitric Oxide, pubmed-meshheading:12485443-Nitric Oxide Synthase, pubmed-meshheading:12485443-Scleroderma, Systemic, pubmed-meshheading:12485443-Skin, pubmed-meshheading:12485443-Substance P, pubmed-meshheading:12485443-Vasodilation, pubmed-meshheading:12485443-Vasodilator Agents
pubmed:year
2002
pubmed:articleTitle
Endothelial dysfunction in murine model of systemic sclerosis: tight-skin mice 1.
pubmed:affiliation
Department of Zoology and Animal Biology, University of Geneva, Sciences III, 30 Quai Ernest Ansermet, 1211 Geneva 4, Switzerland. Isabelle.marie@chu-rouen.fr
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't