Linked Life Data

18642698

Source:http://linkedlifedata.com/resource/pubmed/id/18642698

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2008-7-22
pubmed:abstractText
We studied the effect of hypoxia on activation and stimulation of apoptosis in cultured endothelial cells. The effect of hypoxia was compared to that of apoptosis-inducing agents (tumor necrosis factor and bacterial lipopolysaccharide). Incubation of endothelial cells for 24 h under hypoxic conditions (2% O2, 5% CO2, and 93% N2) increased secretion of von Willebrand factor, but had no effect on the expression of cell adhesion molecule ICAM-1. Tumor necrosis factor and lipopolysaccharide did not stimulate secretion of von Willebrand factor, but significantly increased the expression of ICAM-1. These data attest to significant differences in the mechanisms of endothelium activation under hypoxic conditions and during treatment with tumor necrosis factor or lipopolysaccharide. Hypoxia stimulated apoptosis in endothelial cells, which was seen from the increase in the number of annexin V-binding cells and activation of caspase-3. Similar changes were revealed in the presence of tumor necrosis factor and lipopolysaccharide. Hence, damage to endothelial cells caused by hypoxia and these compounds is mediated by similar mechanisms.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0007-4888
pubmed:author
pubmed:issnType
Print
pubmed:volume
144
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
504-6
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Damage and activation of endothelial cells during in vitro hypoxia.
pubmed:affiliation
Institute of Experimental Cardiology, Russian Cardiology Research and Production Complex, Russian Ministry of Health, Moscow.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't