Linked Life Data

11726405

Source:http://linkedlifedata.com/resource/pubmed/id/11726405

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2001-11-29
pubmed:abstractText
Leukocyte infiltration is known to play an important role in hypoxia-induced tissue damage. There is a paucity of information on the role of hypoxia in the expression of adhesion molecules on respiratory epithelial cells. The current studies focus on the adhesion molecules intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), their expression pattern on alveolar epithelial cells, and their biologic function under hypoxic conditions. Rat alveolar epithelial cells (AEC) were exposed to hypoxia for several time periods. With 5% oxygen, mRNA for ICAM-1 and VCAM-1 rose by 100%, peaking between 0.5 and 1 h. ICAM-1 and VCAM-1 protein showed an increase between 2 and 4 h. Neutrophil adherence to hypoxia-exposed AEC was enhanced by 115%. This increase was reduced by 83% with anti-ICAM-1 antibody. Adherence of alveolar macrophages to AEC increased by 118% and could be blocked by 95% with anti-VCAM-1 antibody. The present study shows for the first time an early increase of ICAM-1 and VCAM-1 expression on rat AEC under hypoxic conditions. These adhesion molecules are involved in increased adhesiveness of neutrophils and macrophages. Such responses might play an important role in the adhesion of leukocytes and macrophages to lung epithelial cells during hypoxic conditions.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1044-1549
pubmed:author
pubmed:issnType
Print
pubmed:volume
25
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
780-7
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Hypoxia mediates increased neutrophil and macrophage adhesiveness to alveolar epithelial cells.
pubmed:affiliation
Institutes of Anesthesiology and Physiology, University of Zurich, Zurich, Switzerland. bbeck@physiol.unizh.ch
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't