Linked Life Data

7532161

Source:http://linkedlifedata.com/resource/pubmed/id/7532161

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1995-3-23
pubmed:abstractText
Cellular adhesion of sialyl-Lewis-a(SLea)-positive pancreas carcinoma to endothelial cells (EC) is augmented by activation of EC via up-regulated E-selectin expression on EC. Co-cultivation of pancreas-carcinoma cells, PCI-24, with human umbilical-vein endothelial cells (HUVEC) for 5 hr at the PCI-to-HUVEC ratio of 1:10 induced E-selectin expression on the endothelial-cell surface, augmenting SLea-positive pancreas-carcinoma cell attachment with HUVEC. Culture supernatants of 6 tested pancreas-carcinoma cell lines contained soluble, E-selectin-inducing factor(s). The E-selectin-inducing effect by the supernatants was blocked by the protein-kinase-C inhibitor, H7. Antibodies against SLea and E-selectin but not SLex or ICAM-1 blocked the increased pancreas-carcinoma-to-endothelial attachment. Paraformaldehyde(PFA)-fixed PCI-24 cells also induced E-selectin on vascular endothelial cells upon direct contact with endothelial cells, indicating the presence of a membrane-bound form. The 6 pancreas-carcinoma lines all produced IL-1 alpha mRNA and protein but not IL-1 beta or TNF-alpha protein and/or mRNA. Absorption of IL-1 alpha from the supernatants by IL-1 alpha-specific antibody almost completely abolished E-selectin-inducing activity. Anti-IL-1 alpha antibody also abolished the E-selectin-inducing activity of PFA-fixed PCI. IL-1 alpha production by PCI cells was up-regulated by TNF-alpha. These observations suggest that substance(s) produced by pancreas-carcinoma cells, in this case, IL-1 alpha, may contribute to pancreas-carcinoma-cell colonization in non-inflamed, distant locations in vivo, by activating vascular endothelial cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0020-7136
pubmed:author
pubmed:issnType
Print
pubmed:day
3
pubmed:volume
60
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
712-7
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:7532161-1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine, pubmed-meshheading:7532161-Carcinoma, pubmed-meshheading:7532161-Cell Adhesion, pubmed-meshheading:7532161-Cell Adhesion Molecules, pubmed-meshheading:7532161-Cell Communication, pubmed-meshheading:7532161-Cells, Cultured, pubmed-meshheading:7532161-Culture Media, Conditioned, pubmed-meshheading:7532161-E-Selectin, pubmed-meshheading:7532161-Endothelium, Vascular, pubmed-meshheading:7532161-Gangliosides, pubmed-meshheading:7532161-Gene Expression Regulation, pubmed-meshheading:7532161-Humans, pubmed-meshheading:7532161-Interleukin-1, pubmed-meshheading:7532161-Isoquinolines, pubmed-meshheading:7532161-Neoplasm Proteins, pubmed-meshheading:7532161-Pancreatic Neoplasms, pubmed-meshheading:7532161-Piperazines, pubmed-meshheading:7532161-Protein Kinase C, pubmed-meshheading:7532161-Stimulation, Chemical, pubmed-meshheading:7532161-Tumor Cells, Cultured, pubmed-meshheading:7532161-Umbilical Veins
pubmed:year
1995
pubmed:articleTitle
E-selectin expression induced by pancreas-carcinoma-derived interleukin-1 alpha results in enhanced adhesion of pancreas-carcinoma cells to endothelial cells.
pubmed:affiliation
Department of Pathology, Hokkaido University School of Medicine, Sapporo, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't