Increased expression and redistribution of the antiapoptotic molecule Bcl-xL in Parkinson's disease.
Identifieur interne : 001147 ( PubMed/Curation ); précédent : 001146; suivant : 001148Increased expression and redistribution of the antiapoptotic molecule Bcl-xL in Parkinson's disease.
Auteurs : Andreas Hartmann [France] ; Annick Mouatt-Prigent ; Miquel Vila ; Nacer Abbas ; Céline Perier ; Baptiste A. Faucheux ; Sheela Vyas ; Etienne C. HirschSource :
- Neurobiology of disease [ 0969-9961 ] ; 2002.
English descriptors
- KwdEn :
- Aged, Aged, 80 and over, Apoptosis (physiology), Dihydroxyphenylalanine (physiology), Humans, Melanins (metabolism), Mesencephalon (metabolism), Mesencephalon (ultrastructure), Neurons (metabolism), Neurons (physiology), Neurons (ultrastructure), Organ Specificity, Parkinson Disease (metabolism), Parkinson Disease (pathology), Proto-Oncogene Proteins c-bcl-2 (biosynthesis), Proto-Oncogene Proteins c-bcl-2 (metabolism), Proto-Oncogene Proteins c-bcl-2 (ultrastructure), RNA, Messenger (biosynthesis), bcl-X Protein.
- MESH :
- chemical , biosynthesis : Proto-Oncogene Proteins c-bcl-2, RNA, Messenger.
- chemical , metabolism : Melanins, Proto-Oncogene Proteins c-bcl-2.
- chemical , physiology : Dihydroxyphenylalanine.
- metabolism : Mesencephalon, Neurons, Parkinson Disease.
- pathology : Parkinson Disease.
- physiology : Apoptosis, Neurons.
- ultrastructure : Mesencephalon, Neurons, Proto-Oncogene Proteins c-bcl-2.
- Aged, Aged, 80 and over, Humans, Organ Specificity, bcl-X Protein.
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.
PubMed: 12079401
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pubmed:12079401Le document en format XML
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<front><div type="abstract" xml:lang="en">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.</div>
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