Linked Life Data

10564170

Source:http://linkedlifedata.com/resource/pubmed/id/10564170

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5 Pt 1
pubmed:dateCreated
1999-12-14
pubmed:abstractText
Accumulation of intraluminal polymorphonuclear leukocytes (PMN) is a hallmark of inflammatory diseases of the airways. Extracellular nucleotides stimulate PMN adhesion to human main pulmonary artery endothelial cells (HPAEC) by a purinoceptor-mediated mechanism. We investigated the effects of nucleotides on adhesion of freshly isolated human PMN to cultured human tracheobronchial epithelial cells (HBEC). We found that extracellular ATP and UTP were much less effective in stimulating PMN adhesion to HBEC compared with HPAEC, whereas the bacterial chemotactic peptide N-formyl-Met-Leu-Phe stimulated PMN adhesion to both cell types to an equal degree. We investigated several mechanisms that might account for decreased nucleotide-induced PMN adhesion to HBEC. The ectonucleotidase-resistant ATP analog adenosine 5'-O-(3-thiotriphosphate) was also ineffective in stimulating PMN adhesion to HBEC, indicating that degradation of ATP by ectonucleotidase(s) was not responsible for altered PMN adhesion. HBEC responded to ATP and UTP with increased intracellular calcium, indicating that these cells are capable of purinoceptor-mediated responses. We found that ATP and UTP also did not stimulate PMN adhesion to Chinese hamster ovary (CHO) cells, which had been stably transfected with the gene for hamster Muc1, a cell-associated mucin. However, ATP and UTP did stimulate adhesion of PMN to nontransfected CHO cells. These results suggested that MUC1 mucin modulates PMN adhesion to epithelium. We found that cultured HBEC expressed more mRNA and protein for MUC1 mucin than did HPAEC. We conclude that extracellular nucleotides are less effective in stimulating PMN adhesion to epithelial cells than to endothelial cells and that overexpression of hamster Muc1 mucin inhibits nucleotide-induced PMN adhesion to CHO cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
277
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
L874-80
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:10564170-Adenosine Triphosphate, pubmed-meshheading:10564170-Animals, pubmed-meshheading:10564170-Blotting, Northern, pubmed-meshheading:10564170-CHO Cells, pubmed-meshheading:10564170-Calcium, pubmed-meshheading:10564170-Cell Adhesion, pubmed-meshheading:10564170-Cells, Cultured, pubmed-meshheading:10564170-Chromium Radioisotopes, pubmed-meshheading:10564170-Cricetinae, pubmed-meshheading:10564170-Endothelium, Vascular, pubmed-meshheading:10564170-Epithelial Cells, pubmed-meshheading:10564170-Gene Expression, pubmed-meshheading:10564170-Humans, pubmed-meshheading:10564170-Mucin-1, pubmed-meshheading:10564170-Neutrophils, pubmed-meshheading:10564170-Peptide Fragments, pubmed-meshheading:10564170-Pulmonary Artery, pubmed-meshheading:10564170-RNA, Messenger, pubmed-meshheading:10564170-Receptors, Purinergic, pubmed-meshheading:10564170-Uridine Triphosphate
pubmed:year
1999
pubmed:articleTitle
Nucleotide-induced PMN adhesion to cultured epithelial cells: possible role of MUC1 mucin.
pubmed:affiliation
Pulmonary/Critical Care Section, Providence Veterans Affairs Medical Center, Brown University School of Medicine, Providence, Rhode Island 02908, USA. sharon_rounds@brown.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't