Show simple item record

dc.contributor.authorRenshaw, Gillianen_US
dc.contributor.authorWarburton, Joshuaen_US
dc.contributor.authorGirjes, Adeepen_US
dc.contributor.editorS Tabibzadehen_US
dc.date.accessioned2017-05-03T12:01:39Z
dc.date.available2017-05-03T12:01:39Z
dc.date.issued2004en_US
dc.date.modified2009-09-25T04:42:53Z
dc.identifier.issn10939946en_US
dc.identifier.urihttp://hdl.handle.net/10072/5505
dc.description.abstractChanges in gene expression are associated with switching to an autoprotected phenotype in response to environmental and physiological stress. Ubiquitous molecular chaperones from the heat shock protein (HSP) superfamily confer neuronal protection that can be blocked by antibodies. Recent research has focused on the interactions between the molecular sensors that affect the increased expression of neuroprotective HSPs above constitutive levels. An examination of the conditions under which the expression of heat shock protein 70 (Hsp70) was up regulated in a hypoxia and anoxia tolerant tropical species, the epaulette shark (Hemiscyllium ocellatum), revealed that up-regulation was dependent on exceeding a stimulus threshold for an oxidative stressor. While hypoxic-preconditioning confers neuroprotective changes, there was no increase in the level of Hsp70 indicating that its increased expression was not associated with achieving a neuroprotected state in response to hypoxia in the epaulette shark. Conversely, there was a significant increase in Hsp70 in response to anoxic-preconditioning, highlighting the presence of a stimulus threshold barrier and raising the possibility that, in this species, Hsp70 contributes to the neuroprotective response to extreme crises, such as oxidative stress. Interestingly, there was a synergistic effect of coincident stressors on Hsp70 expression, which was revealed when metabolic stress was superimposed upon oxidative stress. Brain energy charge was significantly lower when adenosine receptor blockade, provided by treatment with aminophylline, was present prior to the final anoxic episode, under these circumstances, the level of Hsp70 induced was significantly higher than in the pair-matched saline treated controls. An understanding of the molecular and metabolic basis for neuroprotective switches, which result in an up-regulation of neuroprotective Hsp70 expression in the brain, is needed so that intervention strategies can be devised to manage CNS pathologies and minimise damage caused by ischemia and trauma. In addition, the current findings indicate that measurements of HSP expression per se may provide a useful correlate of the level of neuroprotection achieved in the switch to an autoprotected phenotype.en_US
dc.description.peerreviewedYesen_US
dc.description.publicationstatusYesen_AU
dc.languageEnglishen_US
dc.language.isoen_AU
dc.publisherFrontiers in Bioscienceen_US
dc.publisher.placeUSAen_US
dc.publisher.urihttp://www.bioscience.org/en_AU
dc.relation.ispartofpagefrom110en_US
dc.relation.ispartofpageto116en_US
dc.relation.ispartofissueJanen_US
dc.relation.ispartofjournalFrontiers in Bioscienceen_US
dc.relation.ispartofvolume9en_US
dc.subject.fieldofresearchHISTORY AND ARCHAEOLOGYen_US
dc.subject.fieldofresearchcode210000en_US
dc.subject.fieldofresearchcode270602en_US
dc.titleOxygen sensors and energy sensors act synergistically to achieve a graded alteration in gene expression: consequences for assessing the level of neuroprotection in response to stressorsen_US
dc.typeJournal articleen_US
dc.type.descriptionC1 - Peer Reviewed (HERDC)en_US
dc.type.codeC - Journal Articlesen_US
gro.date.issued2004
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