{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Krishnamoorthy S"],"funding":["NIGMS NIH HHS"],"pagination":["2018-27"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3349829"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["180(5)"],"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"],"journal":["The American journal of pathology"],"pubmed_title":["Resolvin D1 receptor stereoselectivity and regulation of inflammation and proresolving microRNAs."],"pmcid":["PMC3349829"],"funding_grant_id":["R01-GM038765","R01 GM038765"],"pubmed_authors":["Fredman G","Recchiuti A","Krishnamoorthy S","Serhan CN","Chiang N"],"additional_accession":[]},"is_claimable":false,"name":"Resolvin D1 receptor stereoselectivity and regulation of inflammation and proresolving microRNAs.","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","dates":{"release":"2012-01-01T00:00:00Z","publication":"2012 May","modification":"2025-04-05T15:41:18.467Z","creation":"2019-03-27T00:53:22Z"},"accession":"S-EPMC3349829","cross_references":{"pubmed":["22449948"],"doi":["10.1016/j.ajpath.2012.01.028"]}}