Abstract
In the present study, we tried to clarify the potentially protective role of Bcl-x(L), an anti-apoptotic member of the Bcl-2 family of proteins, in Parkinson's disease (PD). Using in situ hybridization on human postmortem mesencephalon sections, we show that in PD patients Bcl-x(L) mRNA expression per dopaminergic neuron was almost double that of controls. We also show that, ultrastructurally, this effect may be mediated by a redistribution of Bcl-x(L) from the cytosol to the outer mitochondrial membrane.
2002 Elsevier Science (USA).
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Aged
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Aged, 80 and over
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Apoptosis / physiology*
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Dihydroxyphenylalanine / physiology
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Humans
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Melanins / metabolism
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Mesencephalon / metabolism
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Mesencephalon / ultrastructure
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Neurons / metabolism
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Neurons / physiology
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Neurons / ultrastructure
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Organ Specificity
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Parkinson Disease / metabolism*
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Parkinson Disease / pathology
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Proto-Oncogene Proteins c-bcl-2 / biosynthesis*
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Proto-Oncogene Proteins c-bcl-2 / metabolism
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Proto-Oncogene Proteins c-bcl-2 / ultrastructure
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RNA, Messenger / biosynthesis
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bcl-X Protein
Substances
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BCL2L1 protein, human
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Melanins
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Proto-Oncogene Proteins c-bcl-2
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RNA, Messenger
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bcl-X Protein
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neuromelanin
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Dihydroxyphenylalanine