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http://purl.uniprot.org/citations/28256515http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/28256515http://www.w3.org/2000/01/rdf-schema#comment"Two distinct monocyte (Mo)/macrophage (Mp) subsets (Ly6Clow and Ly6Chigh) orchestrate cardiac recovery process following myocardial infarction (MI). Prostaglandin (PG) E2 is involved in the Mo/Mp-mediated inflammatory response, however, the role of its receptors in Mos/Mps in cardiac healing remains to be determined. Here we show that pharmacological inhibition or gene ablation of the Ep3 receptor in mice suppresses accumulation of Ly6Clow Mos/Mps in infarcted hearts. Ep3 deletion in Mos/Mps markedly attenuates healing after MI by reducing neovascularization in peri-infarct zones. Ep3 deficiency diminishes CX3C chemokine receptor 1 (CX3CR1) expression and vascular endothelial growth factor (VEGF) secretion in Mos/Mps by suppressing TGFβ1 signalling and subsequently inhibits Ly6Clow Mos/Mps migration and angiogenesis. Targeted overexpression of Ep3 receptors in Mos/Mps improves wound healing by enhancing angiogenesis. Thus, the PGE2/Ep3 axis promotes cardiac healing after MI by activating reparative Ly6Clow Mos/Mps, indicating that Ep3 receptor activation may be a promising therapeutic target for acute MI."xsd:string
http://purl.uniprot.org/citations/28256515http://purl.org/dc/terms/identifier"doi:10.1038/ncomms14656"xsd:string
http://purl.uniprot.org/citations/28256515http://purl.uniprot.org/core/author"Chen G."xsd:string
http://purl.uniprot.org/citations/28256515http://purl.uniprot.org/core/author"Liu G."xsd:string
http://purl.uniprot.org/citations/28256515http://purl.uniprot.org/core/author"Shen Y."xsd:string
http://purl.uniprot.org/citations/28256515http://purl.uniprot.org/core/author"Wang J."xsd:string
http://purl.uniprot.org/citations/28256515http://purl.uniprot.org/core/author"Zhang J."xsd:string
http://purl.uniprot.org/citations/28256515http://purl.uniprot.org/core/author"Qin J."xsd:string
http://purl.uniprot.org/citations/28256515http://purl.uniprot.org/core/author"Yu Y."xsd:string
http://purl.uniprot.org/citations/28256515http://purl.uniprot.org/core/author"Wang K."xsd:string
http://purl.uniprot.org/citations/28256515http://purl.uniprot.org/core/author"Tang J."xsd:string
http://purl.uniprot.org/citations/28256515http://purl.uniprot.org/core/author"Lazarus M."xsd:string
http://purl.uniprot.org/citations/28256515http://purl.uniprot.org/core/author"Zuo S."xsd:string
http://purl.uniprot.org/citations/28256515http://purl.uniprot.org/core/author"Wan Q."xsd:string
http://purl.uniprot.org/citations/28256515http://purl.uniprot.org/core/author"Tao B."xsd:string
http://purl.uniprot.org/citations/28256515http://purl.uniprot.org/core/author"Yu Y.'"xsd:string
http://purl.uniprot.org/citations/28256515http://purl.uniprot.org/core/date"2017"xsd:gYear
http://purl.uniprot.org/citations/28256515http://purl.uniprot.org/core/name"Nat Commun"xsd:string
http://purl.uniprot.org/citations/28256515http://purl.uniprot.org/core/pages"14656"xsd:string
http://purl.uniprot.org/citations/28256515http://purl.uniprot.org/core/title"Activation of E-prostanoid 3 receptor in macrophages facilitates cardiac healing after myocardial infarction."xsd:string
http://purl.uniprot.org/citations/28256515http://purl.uniprot.org/core/volume"8"xsd:string
http://purl.uniprot.org/citations/28256515http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/28256515
http://purl.uniprot.org/citations/28256515http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/28256515
http://purl.uniprot.org/uniprot/#_A0A077S2U6-mappedCitation-28256515http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/28256515