Endoplasmic Reticulum Calcium Release Engages Bax Translocation in Cortical Astrocytes

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dc.contributor.author Morales, A. P.
dc.contributor.author Carvalho, A. C. P.
dc.contributor.author Monteforte, P. T.
dc.contributor.author Hirata, H.
dc.contributor.author Han, S. W. [UNIFESP]
dc.contributor.author Hsu, Y. -T.
dc.contributor.author Smaili, Soraya Soubhi [UNIFESP]
dc.date.accessioned 2016-01-24T14:16:42Z
dc.date.available 2016-01-24T14:16:42Z
dc.date.issued 2011-05-01
dc.identifier http://dx.doi.org/10.1007/s11064-011-0411-8
dc.identifier.citation Neurochemical Research. New York: Springer/plenum Publishers, v. 36, n. 5, p. 829-838, 2011.
dc.identifier.issn 0364-3190
dc.identifier.uri http://repositorio.unifesp.br/handle/11600/33670
dc.description.abstract Apoptosis is a highly complex form of cell death that can be triggered by alterations in Ca(2+) homeostasis. Members of the Bcl-2 family may regulate apoptosis and modulate Ca(2+) distribution within intracellular compartments. Bax, a proapoptotic member of the family, is constitutively expressed and soluble in the cytosol and, under apoptotic induction, translocates to mitochondrial membranes. However, it is not clear if the intracellular Ca(2+) stores and selective Ca(2+) releases can modulate or control Bax translocation. the aim of this study was to investigate the relation of intracellular Ca(2+) stores with Bax translocation in rat cortical astrocytes. Results show that the classical apoptotic inducer, staurosporine, caused high elevations of cytosolic Ca(2+) that precede Bax translocation. On the other hand, agents that mobilize Ca(2+) from endoplasmic reticulum such as noradrenaline or thapsigargin, induced Bax translocation, while mitochondrial Ca(2+) release evoked by carbonyl cyanide-p-(trifluoromethoxyphenyl) hydrazone was not able to cause Bax punctation. in addition, microinjection of inositol 1,4,5- trisphosphate induced Bax translocation. Taken together, our results show that in Bax overexpressing cortical astrocytes, endoplasmic reticulum-Ca(2+) release may induce Bax transactivation and specifically control apoptosis. en
dc.description.sponsorship Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorship Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorship NIH
dc.format.extent 829-838
dc.language.iso eng
dc.publisher Springer
dc.relation.ispartof Neurochemical Research
dc.rights Acesso restrito
dc.subject Bax en
dc.subject Calcium en
dc.subject Endoplasmic reticulum en
dc.subject Mitochondria en
dc.subject Apoptosis en
dc.subject Astrocytes en
dc.subject Rat en
dc.subject Cell death en
dc.title Endoplasmic Reticulum Calcium Release Engages Bax Translocation in Cortical Astrocytes en
dc.type Artigo
dc.rights.license http://www.springer.com/open+access/authors+rights?SGWID=0-176704-12-683201-0
dc.contributor.institution Universidade Federal de São Paulo (UNIFESP)
dc.contributor.institution Med Univ S Carolina
dc.description.affiliation Universidade Federal de São Paulo UNIFESP EPM, Dept Biofis, BR-04044020 São Paulo, Brazil
dc.description.affiliation Med Univ S Carolina, Dept Biochem & Mol Biol, Charleston, SC 29425 USA
dc.description.affiliation Universidade Federal de São Paulo UNIFESP EPM, Dept Farmacol, Escola Paulista Med, BR-04044020 São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo UNIFESP EPM, Dept Biofis, BR-04044020 São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo UNIFESP EPM, Dept Farmacol, Escola Paulista Med, BR-04044020 São Paulo, Brazil
dc.description.sponsorshipID NIH: NS40932
dc.identifier.doi 10.1007/s11064-011-0411-8
dc.description.source Web of Science
dc.identifier.wos WOS:000289215000017



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