Disrupted mitochondrial electron transport function increases expression of anti‐apoptotic Bcl‐2 and Bcl‐XL proteins in SH‐SY5Y neuroblastoma and in Parkinson disease cybrid cells through oxidative stress
Identifieur interne : 001C43 ( Main/Exploration ); précédent : 001C42; suivant : 001C44Disrupted mitochondrial electron transport function increases expression of anti‐apoptotic Bcl‐2 and Bcl‐XL proteins in SH‐SY5Y neuroblastoma and in Parkinson disease cybrid cells through oxidative stress
Auteurs : George A. Veech [États-Unis] ; Jameel Dennis [États-Unis] ; Paula M. Keeney [États-Unis] ; Christopher P. Fall [États-Unis] ; Russell H. Swerdlow [États-Unis] ; W. Davis Parker Jr. [États-Unis] ; James P. Bennett Jr. [États-Unis]Source :
- Journal of Neuroscience Research [ 0360-4012 ] ; 2000-09-15.
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Abstract
Death of dopamine neurons in Parkinson disease (PD) may arise from consequences of the complex I (C‐I) defect in the mitochondrial electron transport chain (ETC). Whether cells activate programmed death (apoptosis) pathways derives, in part, from relative activities of proteins such as bcl‐2 and bcl‐XL , that have anti‐apoptotic actions. We studied the responses of bcl‐2 and bcl‐XL genes in pharmacologic (acute incubation with methylpyridinium (MPP+)) and mitochondrial transgenic (“cybrid”) models of Parkinson disease C‐I defects. MPP+ incubation increased levels of bcl‐2 and bcl‐XL proteins in native SH‐SY5Y cells but not in ρ0 cells devoid of ETC activity. MPP+ increased bcl‐2 mRNA levels by 40% at 8 hr. Confocal microscopic imaging showed that the intracellular distribution of immunoreactive bcl‐2 was not significantly associated with mitochondrial membranes at baseline but was associated with mitochondria after 12 hr of MPP+. Immunoreactive bcl‐XL protein was significantly and equally associated with mitochondrial membranes both at baseline and after MPP+. PD cybrids showed increased basal levels of bcl‐2 and bcl‐XL proteins, similar to the maximum levels found after MPP+ treatment of control SY5Y cells. After MPP+ exposure, bcl‐2 protein levels increased in control cybrids but did not increase further in PD cybrids. Both pharmacologically generated and transgenically induced C‐I inhibition increases levels of anti‐apoptotic bcl proteins, possibly from increased gene transcription. Augmentation of bcl‐2 and bcl‐XL expression may delay neurodegeneration in PD. J. Neurosci. Res. 61:693–700, 2000. © 2000 Wiley‐Liss, Inc.
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DOI: 10.1002/1097-4547(20000915)61:6<693::AID-JNR13>3.0.CO;2-4
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Whether cells activate programmed death (apoptosis) pathways derives, in part, from relative activities of proteins such as bcl‐2 and bcl‐XL , that have anti‐apoptotic actions. We studied the responses of bcl‐2 and bcl‐XL genes in pharmacologic (acute incubation with methylpyridinium (MPP+)) and mitochondrial transgenic (“cybrid”) models of Parkinson disease C‐I defects. MPP+ incubation increased levels of bcl‐2 and bcl‐XL proteins in native SH‐SY5Y cells but not in ρ0 cells devoid of ETC activity. MPP+ increased bcl‐2 mRNA levels by 40% at 8 hr. Confocal microscopic imaging showed that the intracellular distribution of immunoreactive bcl‐2 was not significantly associated with mitochondrial membranes at baseline but was associated with mitochondria after 12 hr of MPP+. Immunoreactive bcl‐XL protein was significantly and equally associated with mitochondrial membranes both at baseline and after MPP+. PD cybrids showed increased basal levels of bcl‐2 and bcl‐XL proteins, similar to the maximum levels found after MPP+ treatment of control SY5Y cells. After MPP+ exposure, bcl‐2 protein levels increased in control cybrids but did not increase further in PD cybrids. Both pharmacologically generated and transgenically induced C‐I inhibition increases levels of anti‐apoptotic bcl proteins, possibly from increased gene transcription. Augmentation of bcl‐2 and bcl‐XL expression may delay neurodegeneration in PD. J. Neurosci. Res. 61:693–700, 2000. © 2000 Wiley‐Liss, Inc.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Virginie</li></region></list><tree><country name="États-Unis"><region name="Virginie"><name sortKey="Veech, George A" sort="Veech, George A" uniqKey="Veech G" first="George A." last="Veech">George A. 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