http://purl.uniprot.org/citations/15001561 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/15001561 | http://www.w3.org/2000/01/rdf-schema#comment | "The aims of the present study were to determine the effects and mechanisms of angiotensin II (Ang II) on leukocyte-endothelium interactions and the role of Ang II in a novel model of ischemia/reperfusion (I/R) in the mouse colon. Ang II dose-dependently increased leukocyte rolling and adhesion in colonic venules. Importantly, Ang II-induced leukocyte rolling was completely inhibited by immunoneutralization of P-selectin, and leukocyte adhesion was abolished in lymphocyte function antigen-1 (LFA-1)-deficient mice. The P-selectin-dependent rolling was found to be a precondition for the subsequent LFA-1-dependent leukocyte adhesion. Moreover, Ang II-induced leukocyte responses involved generation of reactive oxygen species and up-regulation of CXC chemokines. Notably, CXC chemokines, but not Ang II, stimulated leukocyte chemotaxis in vitro. I/R increased gene expression of angiotensin converting enzyme (ACE) in the colon and plasma concentrations of Ang II. Inhibition of ACE and the type 1 angiotensin (AT1) receptor significantly decreased the I/R-induced leukocyte adhesion. Taken together, these novel findings demonstrate that Ang II exerts potent pro-inflammatory effects in the colonic microcirculation and that inhibition of Ang II expression or function protects against I/R-induced leukocyte responses in the colon. Thus, it is suggested that Ang II is a major target to control pathological inflammation in the colon."xsd:string |
http://purl.uniprot.org/citations/15001561 | http://purl.org/dc/terms/identifier | "doi:10.1096/fj.03-0502fje"xsd:string |
http://purl.uniprot.org/citations/15001561 | http://purl.uniprot.org/core/author | "Sato T."xsd:string |
http://purl.uniprot.org/citations/15001561 | http://purl.uniprot.org/core/author | "Wang Y."xsd:string |
http://purl.uniprot.org/citations/15001561 | http://purl.uniprot.org/core/author | "Menger M.D."xsd:string |
http://purl.uniprot.org/citations/15001561 | http://purl.uniprot.org/core/author | "Schramm R."xsd:string |
http://purl.uniprot.org/citations/15001561 | http://purl.uniprot.org/core/author | "Thorlacius H."xsd:string |
http://purl.uniprot.org/citations/15001561 | http://purl.uniprot.org/core/author | "Riaz A.A."xsd:string |
http://purl.uniprot.org/citations/15001561 | http://purl.uniprot.org/core/author | "Jeppsson B."xsd:string |
http://purl.uniprot.org/citations/15001561 | http://purl.uniprot.org/core/date | "2004"xsd:gYear |
http://purl.uniprot.org/citations/15001561 | http://purl.uniprot.org/core/name | "FASEB J"xsd:string |
http://purl.uniprot.org/citations/15001561 | http://purl.uniprot.org/core/pages | "881-883"xsd:string |
http://purl.uniprot.org/citations/15001561 | http://purl.uniprot.org/core/title | "Role of angiotensin II in ischemia/reperfusion-induced leukocyte-endothelium interactions in the colon."xsd:string |
http://purl.uniprot.org/citations/15001561 | http://purl.uniprot.org/core/volume | "18"xsd:string |
http://purl.uniprot.org/citations/15001561 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/15001561 |
http://purl.uniprot.org/citations/15001561 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/15001561 |
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