<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Pluskota E</submitter><funding>NIDDK NIH HHS</funding><funding>NHLBI NIH HHS</funding><pagination>3970-8</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC1895095</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>106(12)</volume><pubmed_abstract>High-throughput genomic technology identified an association between a single nucleotide polymorphism (SNP), a proline (P387) rather than the predominant alanine (A387) at position 387 in thrombospondin-4 (TSP-4) and premature myocardial infarction. The inflammatory hypothesis of atherosclerosis invokes a prominent role of leukocytes and cytokines in pathogenesis. As the expression of TSP-4 by vascular cells permits its exposure to circulating leukocytes, the interactions of human neutrophils (polymorphonuclear leukocytes [PMNs]) with both TSP-4 variants were investigated. Phorbol 12-myristate 13-acetate (PMA)-stimulated PMNs adhered and migrated well and equally on the TSP-4 variants. Integrin alpha(M)beta2 was identified as the TSP-4 receptor mediating these responses, and the 3 epiderma</pubmed_abstract><journal>Blood</journal><pubmed_title>Mechanism and effect of thrombospondin-4 polymorphisms on neutrophil function.</pubmed_title><pmcid>PMC1895095</pmcid><funding_grant_id>R01 HL 66197</funding_grant_id><funding_grant_id>K01DK62128</funding_grant_id><funding_grant_id>P50 HL-077107</funding_grant_id><pubmed_authors>Pluskota E</pubmed_authors><pubmed_authors>Topol EJ</pubmed_authors><pubmed_authors>Stenina OI</pubmed_authors><pubmed_authors>Krukovets I</pubmed_authors><pubmed_authors>Szpak D</pubmed_authors><pubmed_authors>Plow EF</pubmed_authors></additional><is_claimable>false</is_claimable><name>Mechanism and effect of thrombospondin-4 polymorphisms on neutrophil function.</name><description>High-throughput genomic technology identified an association between a single nucleotide polymorphism (SNP), a proline (P387) rather than the predominant alanine (A387) at position 387 in thrombospondin-4 (TSP-4) and premature myocardial infarction. The inflammatory hypothesis of atherosclerosis invokes a prominent role of leukocytes and cytokines in pathogenesis. As the expression of TSP-4 by vascular cells permits its exposure to circulating leukocytes, the interactions of human neutrophils (polymorphonuclear leukocytes [PMNs]) with both TSP-4 variants were investigated. Phorbol 12-myristate 13-acetate (PMA)-stimulated PMNs adhered and migrated well and equally on the TSP-4 variants. Integrin alpha(M)beta2 was identified as the TSP-4 receptor mediating these responses, and the 3 epiderma</description><dates><release>2005-01-01T00:00:00Z</release><publication>2005 Dec</publication><modification>2025-04-22T04:48:59.163Z</modification><creation>2019-06-06T14:37:01Z</creation></dates><accession>S-EPMC1895095</accession><cross_references><pubmed>16099885</pubmed><doi>10.1182/blood-2005-03-1292</doi></cross_references></HashMap>