<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Krishnamoorthy S</submitter><funding>NIGMS NIH HHS</funding><pagination>2018-27</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3349829</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>180(5)</volume><pubmed_abstract>Resolution of acute inflammation is an active process that involves the biosynthesis of specialized proresolving lipid mediators. Among them, resolvin D1 (RvD1) actions are mediated by two G protein-coupled receptors (GPCRs), ALX/FPR2 and GPR32, that also regulate specific microRNAs (miRNAs) and their target genes in novel resolution circuits. We report the ligand selectivity of RvD1 activation of ALX/FPR2 and GPR32. In addition to RvD1, its aspirin-triggered epimer and RvD1 analogs each dose dependently and effectively activated ALX/FPR2 and GPR32 in GPCR-overexpressing β-arrestin systems using luminescence and electric cell-substrate impedance sensing. To corroborate these findings in vivo, neutrophil infiltration in self-limited peritonitis was reduced in human ALX/FPR2-overexpressing t</pubmed_abstract><journal>The American journal of pathology</journal><pubmed_title>Resolvin D1 receptor stereoselectivity and regulation of inflammation and proresolving microRNAs.</pubmed_title><pmcid>PMC3349829</pmcid><funding_grant_id>R01-GM038765</funding_grant_id><funding_grant_id>R01 GM038765</funding_grant_id><pubmed_authors>Fredman G</pubmed_authors><pubmed_authors>Recchiuti A</pubmed_authors><pubmed_authors>Krishnamoorthy S</pubmed_authors><pubmed_authors>Serhan CN</pubmed_authors><pubmed_authors>Chiang N</pubmed_authors></additional><is_claimable>false</is_claimable><name>Resolvin D1 receptor stereoselectivity and regulation of inflammation and proresolving microRNAs.</name><description>Resolution of acute inflammation is an active process that involves the biosynthesis of specialized proresolving lipid mediators. Among them, resolvin D1 (RvD1) actions are mediated by two G protein-coupled receptors (GPCRs), ALX/FPR2 and GPR32, that also regulate specific microRNAs (miRNAs) and their target genes in novel resolution circuits. We report the ligand selectivity of RvD1 activation of ALX/FPR2 and GPR32. In addition to RvD1, its aspirin-triggered epimer and RvD1 analogs each dose dependently and effectively activated ALX/FPR2 and GPR32 in GPCR-overexpressing β-arrestin systems using luminescence and electric cell-substrate impedance sensing. To corroborate these findings in vivo, neutrophil infiltration in self-limited peritonitis was reduced in human ALX/FPR2-overexpressing t</description><dates><release>2012-01-01T00:00:00Z</release><publication>2012 May</publication><modification>2025-04-05T15:41:18.467Z</modification><creation>2019-03-27T00:53:22Z</creation></dates><accession>S-EPMC3349829</accession><cross_references><pubmed>22449948</pubmed><doi>10.1016/j.ajpath.2012.01.028</doi></cross_references></HashMap>