Show simple item record

dc.contributor.authorB. Urmaliya, Vijayen_US
dc.contributor.authorE. Church, Jarroden_US
dc.contributor.authorM. Coupar, Ianen_US
dc.contributor.authorRose'Meyer, Roselynen_US
dc.contributor.authorW. Pouton, Colinen_US
dc.contributor.authorJ. White, Paulen_US
dc.contributor.editorMichael R Rosenen_US
dc.date.accessioned2017-04-24T10:25:09Z
dc.date.available2017-04-24T10:25:09Z
dc.date.issued2009en_US
dc.date.modified2010-05-21T06:37:08Z
dc.identifier.issn01602446en_US
dc.identifier.doi10.1097/FJC.0b013e3181a443e2en_AU
dc.identifier.urihttp://hdl.handle.net/10072/29784
dc.description.abstractExtracellular adenosine concentrations increase within the heart during ischemia, and any exogenous adenosine receptor agonists therefore work in the context of significant local agonist concentrations. We evaluated the interactions between A1, A2A, A2B, and A3 receptors in the presence and absence of adenosine deaminase (ADA, which is used to remove endogenous adenosine) in a cardiac cell ischemia model. Simulated ischemia (SI) was induced by incubating H9c2(2-1) cells in SI medium for 12 hours in 100% N2 gas before assessment of necrosis using propidium iodide (5 卩 or apoptosis using AnnexinV-PE flow cytometry. N6-Cyclopentyladenosine (CPA; 10-7M) and N6-(3-iodobenzyl) adenosine-5'-N-methyluronamide (IB-MECA; 10-7M) reduced the proportion of nonviable cells to 30.87 ᠲ.49% and 35.18 ᠱ0.30%, respectively (% of SI group). In the presence of ADA, the protective effect of CPA was reduced (62.82 ᠳ.52% nonviable), whereas the efficacy of IB-MECA was unchanged (35.81 ᠳ.84% nonviable; P < 0.05, n = 3-5, SI vs. SI + ADA). The protective effects of CPA and IB-MECA were abrogated in the presence of their respective antagonists DPCPX (8-cyclopentyl-1,3-dipropylxanthine) and MRS1191 [3-ethyl-5-benzyl-2-methyl-4-phenylethynyl-6-phenyl-1,4-(ᩭdihydropyridine-3,5-dicarboxylate], whereas A2A and A2B agonists had no significant effect. CPA-mediated protection was abrogated in the presence of both A2A (ZM241385, 4-(2-[7-amino-2-(2-furyl)[1,2,4]triazolo[2,3-a][1,3,5]triazin-5-lamino]ethyl)phenol; 50 nM) and A2B (MRS1754, 8-[4-[((4-cyanophenyl)carbamoylmethyl)oxy]phenyl]-1,3-di(n-propyl)xanthine; 200 nM) antagonists (n = 3-5, P < 0.05). In the absence of endogenous adenosine, significant protection was observed with CPA in presence of CGS21680 (4-[2-[[6-amino-9-(N-ethyl-b-d-ribofuranuronamidosyl)-9H-purin-2-yl]amino]ethyl]benzenepropanoic acid) or LUF5834 [2-amino-4-(4-hydroxyphenyl)-6-(1H-imidazol-2-ylmethylsulfanyl)pyridine-3,5-dicarbonitrile] (P < 0.05 vs. SI + ADA + CPA). Apoptosis (14.35 ᠰ.15% of cells in SI + ADA group; P < 0.05 vs. control) was not significantly reduced by CPA or IB-MECA. In conclusion, endogenous adenosine makes a significant contribution to A1 agonist-mediated prevention of necrosis in this SI model by cooperative interactions with both A2A and A2B receptors but does not play a role in A3 agonist-mediated protection.en_US
dc.description.peerreviewedYesen_US
dc.description.publicationstatusYesen_AU
dc.languageEnglishen_US
dc.language.isoen_AU
dc.publisherLippincott Williams & Wilkinsen_US
dc.publisher.placeUnited Statesen_US
dc.publisher.urihttp://journals.lww.com/cardiovascularpharm/pages/default.aspxen_AU
dc.relation.ispartofstudentpublicationYen_AU
dc.relation.ispartofpagefrom424en_US
dc.relation.ispartofpageto433en_US
dc.relation.ispartofissue5en_US
dc.relation.ispartofjournalJournal of Cardiovascular Pharmacologyen_US
dc.relation.ispartofvolume53en_US
dc.rights.retentionYen_AU
dc.subject.fieldofresearchBasic Pharmacologyen_US
dc.subject.fieldofresearchcode111501en_US
dc.titleCardioprotection induced by adenosine A1 receptor agonists in a cardiac cell ischemia model involves cooperative activation of adenosine A2A and A2B receptors by endogenous adenosineen_US
dc.typeJournal articleen_US
dc.type.descriptionC1 - Peer Reviewed (HERDC)en_US
dc.type.codeC - Journal Articlesen_US
gro.date.issued2009
gro.hasfulltextNo Full Text


Files in this item

FilesSizeFormatView

There are no files associated with this item.

This item appears in the following Collection(s)

  • Journal articles
    Contains articles published by Griffith authors in scholarly journals.

Show simple item record