| pubmed-article:9350300 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9350300 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:9350300 | lifeskim:mentions | umls-concept:C1609432 | lld:lifeskim |
| pubmed-article:9350300 | lifeskim:mentions | umls-concept:C0019868 | lld:lifeskim |
| pubmed-article:9350300 | lifeskim:mentions | umls-concept:C0032174 | lld:lifeskim |
| pubmed-article:9350300 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:9350300 | pubmed:dateCreated | 1997-11-19 | lld:pubmed |
| pubmed-article:9350300 | pubmed:abstractText | Various molecules expressed on the surface of platelets have been shown to mediate the protective or deleterious role of these cells in immuno-inflammatory mechanisms. Increasing evidence points to the involvement of the cell adhesion molecules, gpIIb-IIIa, P-selectin, CD31, LFA-1, and CD36 in the interaction between platelets and endothelial cells as well as other cell types. The possible role of these molecules in the ability of platelets to support endothelium and to protect against tumour necrosis factor mediated cytolysis or parasitic invasion are reviewed. The involvement of platelets as effectors of tissue damage in cerebral malaria, lipopolysaccharide induced pathology, and pulmonary fibrosis is also discussed. This has then been extended to include the intercellular mechanisms underpinning their pathogenic role in metastasis, transplant rejection, stroke, brain hypoxia, and related conditions. A better understanding of the complex regulation and hierarchical organisation of these various platelet adhesion molecules may prove useful in the development of new approaches to the treatment of such diseases. | lld:pubmed |
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