Show simple item record

dc.contributor.authorWilliams-Pritchard, Granten_US
dc.contributor.authorPeart, Jasonen_US
dc.contributor.authorHeadrick, Johnen_US
dc.date.accessioned2017-05-03T11:16:47Z
dc.date.available2017-05-03T11:16:47Z
dc.date.issued2009en_US
dc.date.modified2010-07-09T03:02:19Z
dc.identifier.urihttp://hdl.handle.net/10072/31495
dc.description.abstractA1 adenosine receptors (A1ARs) and {delta}-opioid receptors ({delta}-ORs) are involved in cardiovascular control, and mediate tissue protection during periods of stress. These G-protein coupled receptors (GPCRs) may employ similar signalling paths to elicit cardioprotection, and our prior studies support interactions between the two classes of GPCR in mediating protection. We further investigated this interaction in cardiac cells, assessing 'cross-regulation' of receptor mRNA expression in addition to signalling 'cross-talk' of kinase effectors downstream of the receptors. Murine HL-1 cardiomyocytes were stimulated with either an A1AR agonist, (100 nM CCPA) or {delta}-OR agonist (1 占BW 373U86) for varying periods (3, 6, 12, or 24 hrs). Quantitative real-time PCR was used to determine time-dependent changes in mRNA expression for A1ARs and {delta}-ORs. Both agonists triggered a transient repression of A1AR transcription, which recovered to baseline by 24 hrs. Transcription of {delta}-ORs also responded to both A1AR and {delta}-OR agonism, albeit in a differing pattern involving initial repression (by =50%) in the first 3- 6 hrs followed by recovery to slightly above baseline levels at 24 hrs. To assess 'cross-talk', at the level of cell signalling, HL-1 cells were again incubated with CCPA or BW 373U86, either alone or in the presence of a selective A1AR or {delta}-OR antagonist (1 占DPCPX or 1 占BNTX, respectively). Both CCPA and BW 373U86 triggered Erk1/2 phosphorylation which, predictably, was blocked by their respective antagonists. Interestingly, however, the A1AR response was abrogated by {delta}-OR antagonism and, conversely, the {delta}-OR response was eliminated by A1AR antagonism. Erk1/2 phosphorylation with either A1AR or {delta}-OR agonsim was abrogated by an EGFR inhibitor (0.5 占AG1478). These data highlight essential cross-talk between the two receptors systems, involving both cross-regulation of receptor mRNA expression, and an essential interaction in regulation of downstream kinase signalling. The nature of these interactions requires further investigation, but may in part involve EGFR signalling. These findings have important implications regarding cardiac actions of both receptors, particularly in terms of cardioprotection during ischemia-reperfusion.en_US
dc.description.publicationstatusYesen_AU
dc.languageEnglishen_US
dc.language.isoen_AU
dc.publisherLippincott Williams & Wilkinsen_US
dc.publisher.place530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USAen_US
dc.relation.ispartofstudentpublicationYen_AU
dc.relation.ispartofconferencenameAmerican Heart Association Annual conferenceen_US
dc.relation.ispartofconferencetitleCirculationen_US
dc.relation.ispartofdatefrom2008-11-08en_US
dc.relation.ispartofdateto2008-11-13en_US
dc.relation.ispartoflocationNew Orleansen_US
dc.rights.retentionYen_AU
dc.subject.fieldofresearchCardiology (incl. Cardiovascular Diseases)en_US
dc.subject.fieldofresearchcode110201en_US
dc.titleTranscriptional and Cell Signaling Cross-Talk between Adenosine and Opioid Receptors in Cardiac Cellsen_US
dc.typeConference outputen_US
dc.type.descriptionE3 - Conference Publications (Extract Paper)en_US
dc.type.codeE - Conference Publicationsen_US
gro.facultyGriffith Health, School of Medical Scienceen_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)

  • Conference outputs
    Contains papers delivered by Griffith authors at national and international conferences.

Show simple item record