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Mitochondrial-dependent apoptosis in Huntington's disease human cybrids

2010Journal article Open access
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dc.contributor.authorFerreira, IL
dc.contributor.authorNascimento, MV
dc.contributor.authorRibeiro, MH
dc.contributor.authorAlmeida, S
dc.contributor.authorCardoso, SM
dc.contributor.authorGrazina, M
dc.contributor.authorPratas, J
dc.contributor.authorSantos, MJ
dc.contributor.authorJanuário, C
dc.contributor.authorOliveira, CR
dc.contributor.authorRego, AC
dc.date.accessioned2010-02-11T14:28:52Z
dc.date.available2010-02-11T14:28:52Z
dc.date.issued2010
dc.description.abstractWe investigated the involvement of mitochondrial-dependent apoptosis in Huntington's disease (HD) vs. control (CTR) cybrids, obtained from the fusion of human platelets with mitochondrial DNA-depleted NT2 cells, and further exposed to 3-nitropropionic acid (3-NP) or staurosporine (STS). Untreated HD cybrids did not exhibit significant modifications in the activity of mitochondrial respiratory chain complexes I-IV or in mtDNA sequence variations suggestive of a primary role in mitochondrial susceptibility in the subpopulation of HD carriers studied. However, a slight decrease in mitochondrial membrane potential and increased formation of intracellular hydroperoxides was observed in HD cybrids under basal conditions. Furthermore, apoptotic nuclei morphology and a moderate increase in caspase-3 activation, as well as increased levels of superoxide ions and hydroperoxides were observed in HD cybrids upon 3-NP or STS treatment. 3-NP-evoked apoptosis in HD cybrids involved cytochrome c and AIF release from mitochondria, which was associated with mitochondrial Bax translocation. CTR cybrids subjected to 3-NP showed increased mitochondrial Bax and Bim levels and the release of AIF, but not cytochrome c, suggesting a different mode of cell death, linked to the loss of membrane integrity. Additionally, increased mitochondrial Bim and Bak levels, and a slight release of cytochrome c in untreated HD cybrids may help to explain their moderate susceptibility to mitochondrial-dependent apoptosispt
dc.identifier.citationExp Neurol. 2010 Jan 14.pt
dc.identifier.urihttp://hdl.handle.net/10400.4/721
dc.language.isoengpt
dc.publisherElsevierpt
dc.subjectApoptosept
dc.subjectDoença de Huntingtonpt
dc.subjectMitocôndriapt
dc.titleMitochondrial-dependent apoptosis in Huntington's disease human cybridspt
dc.typejournal article
dspace.entity.typePublication
rcaap.rightsopenAccesspt
rcaap.typearticlept

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