Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2002-9-16
pubmed:abstractText
Neutrophil adherence to tumor necrosis factor-alpha (TNF-alpha)-treated human pulmonary microvascular endothelial cells (PMECs) induces cytoskeletal changes in endothelial cells that require intercellular adhesion molecule-1 (ICAM-1)-dependent signaling events. This study determined whether similar changes occurred in rat PMECs and whether rat pulmonary arterial endothelial cells (PAECs) responded differently. Neutrophil adherence induced an increase in the formation of F-actin and in the apparent stiffness of TNF-alpha-treated rat PMECs. These responses, however, were absent in PAECs. To determine the mechanisms underlying these differences, ICAM-1-mediated signaling events were compared. Upregulation of ICAM-1 by TNF-alpha and redistribution of ICAM-1 induced by cross-linking antibodies were similar in both cell types. However, neutrophil adherence induced production of reactive oxygen species only in PMECs and not in PAECs. Moreover, phosphorylation of p38 mitogen-activated protein kinase induced by ICAM-1 cross-linking occurred only in PMECs and not in PAECs. This increase in p38 phosphorylation in PMECs was inhibited by allopurinol, a xanthine oxidase inhibitor. These data demonstrated that whereas TNF-alpha upregulated ICAM-1 and ICAM-1 cross-linking induced a similar redistribution of ICAM-1 on the endothelial cell surface, ICAM-1 ligation initiated p38 activation and cytoskeletal rearrangements only in PMECs and not in PAECs. Thus, neutrophil adhesion through ICAM-1 induced signaling events leading to cytoskeletal changes only in PMECs, the site of neutrophil emigration and edema formation, and not in PAECs.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1073-449X
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
166
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
872-7
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:12231500-Actins, pubmed-meshheading:12231500-Analysis of Variance, pubmed-meshheading:12231500-Animals, pubmed-meshheading:12231500-Biomechanics, pubmed-meshheading:12231500-Cell Adhesion, pubmed-meshheading:12231500-Cell Movement, pubmed-meshheading:12231500-Cells, Cultured, pubmed-meshheading:12231500-Cytoskeleton, pubmed-meshheading:12231500-Data Interpretation, Statistical, pubmed-meshheading:12231500-Endothelium, Vascular, pubmed-meshheading:12231500-Enzyme Activation, pubmed-meshheading:12231500-Fluorescence, pubmed-meshheading:12231500-Humans, pubmed-meshheading:12231500-Inflammation, pubmed-meshheading:12231500-Intercellular Adhesion Molecule-1, pubmed-meshheading:12231500-Lung, pubmed-meshheading:12231500-Microcirculation, pubmed-meshheading:12231500-Mitogen-Activated Protein Kinases, pubmed-meshheading:12231500-Neutrophils, pubmed-meshheading:12231500-Phosphorylation, pubmed-meshheading:12231500-Pulmonary Artery, pubmed-meshheading:12231500-Rats, pubmed-meshheading:12231500-Time Factors, pubmed-meshheading:12231500-Xanthine Oxidase
pubmed:year
2002
pubmed:articleTitle
Lung microvascular and arterial endothelial cells differ in their responses to intercellular adhesion molecule-1 ligation.
pubmed:affiliation
Division of Integrative Biology, Department of Pediatrics, Rainbow Babies and Children's Hospital and Case Western Reserve University, Cleveland, Ohio 44106, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't