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http://purl.uniprot.org/citations/21398608http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/21398608http://www.w3.org/2000/01/rdf-schema#comment"The importance of proresolving mediators in the overall context of the resolution of acute inflammation is well recognized, although little is known about whether these anti-inflammatory and proresolving molecules act in concert. In this article, we focused on lipoxin A(4) (LXA(4)) and annexin A1 (AnxA1) because these two very different mediators converge on a single receptor, formyl peptide receptor type 2 (FPR2/ALX). Addition of LXA(4) to human polymorphonuclear leukocytes (PMNs) provoked a concentration- and time-dependent mobilization of AnxA1 onto the plasma membrane, as determined by Western blotting and flow cytometry analyses. This property was shared by another FPR2/ALX agonist, antiflammin-2, and partly by fMLF or peptide Ac2-26 (an AnxA1 derivative that can activate all three members of the human FPR family). An FPR2/ALX antagonist blocked AnxA1 mobilization activated by LXA(4) and antiflammin-2. Analysis of PMN degranulation patterns and phospho-AnxA1 status suggested a model in which the two FPR2/ALX agonists mobilize the cytosolic (and not the granular) pool of AnxA1 through an intermediate phosphorylation step. Intravital microscopy investigations of the inflamed mesenteric microvasculature of wild-type and AnxA1(-/-) mice revealed that LXA(4) provoked leukocyte detachment from the postcapillary venule endothelium in the former (>50% within 10 min; p < 0.05), but not the latter genotype (∼15%; NS). Furthermore, recruitment of Gr1(+) cells into dorsal air-pouches, inflamed with IL-1β, was significantly attenuated by LXA(4) in wild-type, but not AnxA1(-/-), mice. Collectively, these data prompt us to propose the existence of an endogenous network in anti-inflammation centered on PMN AnxA1 and activated by selective FPR2/ALX agonists."xsd:string
http://purl.uniprot.org/citations/21398608http://purl.org/dc/terms/identifier"doi:10.4049/jimmunol.1003145"xsd:string
http://purl.uniprot.org/citations/21398608http://purl.uniprot.org/core/author"Perretti M."xsd:string
http://purl.uniprot.org/citations/21398608http://purl.uniprot.org/core/author"Flower R.J."xsd:string
http://purl.uniprot.org/citations/21398608http://purl.uniprot.org/core/author"Dalli J."xsd:string
http://purl.uniprot.org/citations/21398608http://purl.uniprot.org/core/author"Cirino G."xsd:string
http://purl.uniprot.org/citations/21398608http://purl.uniprot.org/core/author"Brancaleone V."xsd:string
http://purl.uniprot.org/citations/21398608http://purl.uniprot.org/core/author"Bena S."xsd:string
http://purl.uniprot.org/citations/21398608http://purl.uniprot.org/core/date"2011"xsd:gYear
http://purl.uniprot.org/citations/21398608http://purl.uniprot.org/core/name"J Immunol"xsd:string
http://purl.uniprot.org/citations/21398608http://purl.uniprot.org/core/pages"4905-4914"xsd:string
http://purl.uniprot.org/citations/21398608http://purl.uniprot.org/core/title"Evidence for an anti-inflammatory loop centered on polymorphonuclear leukocyte formyl peptide receptor 2/lipoxin A4 receptor and operative in the inflamed microvasculature."xsd:string
http://purl.uniprot.org/citations/21398608http://purl.uniprot.org/core/volume"186"xsd:string
http://purl.uniprot.org/citations/21398608http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/21398608
http://purl.uniprot.org/citations/21398608http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/21398608
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http://purl.uniprot.org/uniprot/#_P10107-mappedCitation-21398608http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21398608
http://purl.uniprot.org/uniprot/#_P25090-mappedCitation-21398608http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21398608
http://purl.uniprot.org/uniprot/#_Q4FK88-mappedCitation-21398608http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21398608
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http://purl.uniprot.org/uniprot/#_P04083-mappedCitation-21398608http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21398608
http://purl.uniprot.org/uniprot/#_Q3US43-mappedCitation-21398608http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21398608