@prefix pubblicazioni: . @prefix unitaDiPersonaleInterno: . @prefix prodotto: . unitaDiPersonaleInterno:MATRICOLA22471 pubblicazioni:autoreCNRDi prodotto:ID4604 . @prefix prodottidellaricerca: . @prefix istituto: . istituto:CDS059 prodottidellaricerca:prodotto prodotto:ID4604 . @prefix modulo: . modulo:ID2651 prodottidellaricerca:prodotto prodotto:ID4604 . @prefix rdf: . @prefix retescientifica: . prodotto:ID4604 rdf:type retescientifica:ProdottoDellaRicerca , prodotto:TIPO1101 . @prefix rdfs: . prodotto:ID4604 rdfs:label "P2 receptors in human heart: upregulation of P2X6 in patients undergoing heart transplantation, interaction with TNFalpha and potential role in myocardial cell death. (Articolo in rivista)"@en . @prefix xsd: . prodotto:ID4604 pubblicazioni:anno "2005-01-01T00:00:00+01:00"^^xsd:gYear ; pubblicazioni:doi "10.1016/j.yjmcc.2005.09.002"^^xsd:string . @prefix skos: . prodotto:ID4604 skos:altLabel "
Banfi C.1, Ferrario S.2, De Vincenti O.3, Ceruti S.4, Fumagalli M.5, Mazzola A.6, D' Ambrosi N.7, Volont\u00E8 C.8, Fratto P.9, Vitali E.10, Burnstock G.11, Beltrami E.12, Parolari A.13, Polvani G.14, Biglioli P.15, Tremoli E.16, Abbracchio M.P.17 (2005)
P2 receptors in human heart: upregulation of P2X6 in patients undergoing heart transplantation, interaction with TNFalpha and potential role in myocardial cell death.
in Journal of Molecular and Cellular Cardiology
"^^rdf:HTML ; pubblicazioni:autori "Banfi C.1, Ferrario S.2, De Vincenti O.3, Ceruti S.4, Fumagalli M.5, Mazzola A.6, D' Ambrosi N.7, Volont\u00E8 C.8, Fratto P.9, Vitali E.10, Burnstock G.11, Beltrami E.12, Parolari A.13, Polvani G.14, Biglioli P.15, Tremoli E.16, Abbracchio M.P.17"^^xsd:string ; pubblicazioni:paginaInizio "929"^^xsd:string ; pubblicazioni:paginaFine "939"^^xsd:string ; pubblicazioni:altreInformazioni "IF =3.872 SCI-JCR 2005"^^xsd:string ; pubblicazioni:numeroVolume "39"^^xsd:string . @prefix ns11: . prodotto:ID4604 pubblicazioni:rivista ns11:ID304635 ; pubblicazioni:numeroFascicolo "6"^^xsd:string ; skos:note "ISI Web of Science (WOS)"^^xsd:string , "PubMe"^^xsd:string , "Scopu"^^xsd:string ; pubblicazioni:affiliazioni "1-6, 12,16,17 = Department of Pharmacological Sciences, University of Milan, Via Balzaretti 9, 20133 Milan, Italy;\n1,13-16 = Monzino Cardiologic Center IRCCS, Milan, Italy;\n7,8 = Fondazione Santa Lucia, Rome, Italy;\n11 = Autonomic Neurosciences Institute, Royal Free and University College Medical School, London, UK;\n9,10 = Niguarda Hospital, Milan, Italy."^^xsd:string ; pubblicazioni:titolo "P2 receptors in human heart: upregulation of P2X6 in patients undergoing heart transplantation, interaction with TNFalpha and potential role in myocardial cell death."^^xsd:string ; prodottidellaricerca:abstract "ATP acts as a neurotransmitter via seven P2X receptor-channels for Na(+) and Ca(2+), and eight G-protein-coupled P2Y receptors. Despite evidence suggesting roles in human heart, the map of myocardial P2 receptors is incomplete, and their involvement in chronic heart failure (CHF) has never received adequate attention. In left myocardia from five to nine control and 5-12 CHF subjects undergoing heart transplantation, we analyzed the full repertoire of P2 receptors and of 10 \\\"orphan\\\" P2Y-like receptors. All known P2Y receptors (i.e. P2Y(1,2,4,6,11,12,13,14)) and two P2Y-like receptors (GPR91 and GPR17) were detected in all subjects. All known P2X(1-7) receptors were also detected; of these, only P2X(6) was upregulated in CHF, as confirmed by quantitative real time-PCR. The potential significance of this change was studied in primary cardiac fibroblasts freshly isolated from young pigs. Exposure of cardiac fibroblasts to ATP or its hydrolysis-resistant-analog benzoylATP induced apoptosis. TNFalpha (a cytokine implicated in CHF progression) exacerbated cell death. Similar effects were induced by ATP and TNFalpha in a murine cardiomyocytic cell line. In cardiac fibroblasts, TNFalpha inhibited the downregulation of P2X(6) mRNA associated to prolonged agonist exposure, suggesting that, by preventing ATP-induced P2X(6) desensitization, TNFalpha may abolish a defense mechanism meant at avoiding Ca(2+) overload and, ultimately, Ca(2+)-dependent cell death. This may provide a basis for P2X(6) upregulation in CHF. In conclusion, we provide the first characterization of P2 receptors in the human heart and suggest that the interaction between TNFalpha and the upregulated P2X(6) receptor may represent a novel pathogenic mechanism in CHF."@en ; prodottidellaricerca:prodottoDi istituto:CDS059 , modulo:ID2651 ; pubblicazioni:autoreCNR unitaDiPersonaleInterno:MATRICOLA22471 . @prefix parolechiave: . prodotto:ID4604 parolechiave:insiemeDiParoleChiave . ns11:ID304635 pubblicazioni:rivistaDi prodotto:ID4604 . parolechiave:insiemeDiParoleChiaveDi prodotto:ID4604 .