Linked Life Data

8900114

Source:http://linkedlifedata.com/resource/pubmed/id/8900114

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
43
pubmed:dateCreated
1996-12-16
pubmed:abstractText
Binding of natural antibodies to endothelial cell plays an important role in hyperacute xenograft rejection between discordant species. Human intravenous immunoglobulins (IVIg) delay this hyperacute rejection, but their mechanisms of action on endothelial cells have to be defined. Here we demonstrate that IVIg dose-dependently prevent thrombin from eliciting cytosolic Ca2+ movements and nitric oxide (NO) production in aortic endothelial cells from guinea pig. The Ca2+ response to thrombin was similarly affected by IVIg whether they were removed or not from the incubation medium before stimulation. Pretreatment by rat natural antibodies also suppress the thrombin-induced Ca2+ peak corresponding to Ca2+ release from intracellular stores but stimulate the subsequent sustained increase in [Ca2+]i and the release of NO. The action of human intravenous immunoglobulins seems to be selective for the thrombin receptor because they do not affect [Ca2+]i and NO responses to endothelin-1 or thapsigargin. However, these antibodies also suppress the first phase of the cytosolic Ca2+ response to ATP, which does not release NO under our experimental conditions. These observations raise the possibility that IVIg selectively interact with targets localized on plasma membrane of endothelial cells for controlling receptor-activated Ca2+ pathways and NO release.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
25
pubmed:volume
271
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
26473-6
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Human immunoglobulins inhibit thrombin-induced Ca2+ movements and nitric oxide production in endothelial cells.
pubmed:affiliation
Department of Pharmacology, URA CNRS 1482, Paris V University, Necker University School of Medicine, 156 rue de Vaugirard, 75015, Paris, France.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't