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dc.contributor.authorHaddad, John J.de
dc.date.accessioned2008-06-17T14:14:15Z-
dc.date.available2008-06-17T14:14:15Z-
dc.date.issued2007-04-10de
dc.identifier.issn1611-2156de
dc.identifier.urihttp://hdl.handle.net/2003/25682-
dc.identifier.urihttp://dx.doi.org/10.17877/DE290R-348-
dc.description.abstractThe cellular and molecular regulation of MAPKs and apoptosis was investigated in a model of hypoxiatolerance. Survival of neurons in Chrysemys picta bellii, an anoxia-tolerant turtle, involves a reduction in energy metabolism. The biochemical/physiological mechanisms of anoxia tolerance have been examined at the level of ion transport and ATP turnover. However, changes in the phosphorylation state of key enzymes and kinases, mainly, MAPKs, may occur during anoxia, thereby reversible protein phosphorylation could be a critical factor and major mechanism of metabolic reorganization for enduring anaerobiosis. If a turtle were to undergo hypoxia akin to that experienced in its native habitat, it was placed in a glass aquarium filled with water to within a half inch of the top. After the turtle was anesthetized, through extended hypoxia or anesthesia, the animal was sacrificed by decapitation. The brain was then excised and placed in anoxic artificial cerebrospinal fluid. Total protein extraction was performed by homogenizing brain in a buffer, followed by threonine and tyrosine phosphorylation determination of MAPKs, and caspase activity. MAPKp38 was decreased after reoxygenation following 1 day and 1 week hypoxia. The effect of hypoxia on the phosphorylation of MAPKERK was biphasic: Enhancement at 5h and inhibition at 6 weeks. Pro-caspases 8/9 were unchanged by hypoxia until increasing at 6 weeks. Both pro-caspases were upregulated by reoxygenation at 1 day or 6 weeks hypoxia. Neither hypoxia nor reoxygenation induced the cleavage of pro-caspases 8/9 into p20 and p10, respectively. Furthermore, hypoxia induced Bax at 3 days and 1 week, and reoxygenation increased Bax - 4-fold at 1 day. Although the expression of Bcl-2 was slightly increased by hypoxia, [Bcl-2] was 3-4-fold smaller in comparison with Bax. These results indicate that hypoxia up-regulates MAPKERK but not MAPKp38; hypoxia/reperfusion increases the expression of caspases and pro-apoptotic cofactors. The patterns of MAPK regulation suggest the significance of these kinases in cellular adaptation to oxygen deprivation with biomedical correlations, and thereby identify novel natural responsive signaling cofactors in Chrysemys picta bellii with potential pharmacologic and clinical applications.en
dc.language.isoende
dc.relation.ispartofseriesEXCLI Journal ; Vol. 6, 2007en
dc.subjectAnoxiaen
dc.subjectApoptosisen
dc.subjectBrainen
dc.subjectCaspaseen
dc.subjectChrysemys pictaen
dc.subjectHypoxiaen
dc.subjectMAPKen
dc.subjectNeuroprotectionen
dc.subjectTurtleen
dc.subject.ddc610-
dc.titleThe Role of Anti- and Pro-apoptotic Cofactors in Hypoxia/Reoxygenation-Dependent Regulation of MAPKs in the Brain of an Anoxia-Tolerant Modelen
dc.typeTextde
dc.type.publicationtypearticlede
dcterms.accessRightsopen access-
eldorado.dnb.zdberstkatid2132560-1-
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