Glial cell line-derived neurotrophic factor (GDNF) gene expression in the human brain: a post mortem in situ hybridization study with special reference to Parkinson's disease.
Identifieur interne : 001E47 ( Ncbi/Curation ); précédent : 001E46; suivant : 001E48Glial cell line-derived neurotrophic factor (GDNF) gene expression in the human brain: a post mortem in situ hybridization study with special reference to Parkinson's disease.
Auteurs : S. Hunot [France] ; V. Bernard ; B. Faucheux ; F. Boissière ; E. Leguern ; C. Brana ; P P Gautris ; J. Guérin ; B. Bloch ; Yves Agid [France] ; E C HirschSource :
- Journal of neural transmission (Vienna, Austria : 1996) [ 0300-9564 ] ; 1996.
English descriptors
- KwdEn :
- MESH :
- chemical , genetics : Nerve Growth Factors, Nerve Tissue Proteins.
- chemical : Glial Cell Line-Derived Neurotrophic Factor.
- metabolism : Brain, Parkinson Disease.
- physiology : Cell Death.
- Aged, Aged, 80 and over, Case-Control Studies, Gene Expression, Humans, In Situ Hybridization.
Abstract
Glial cell line-derived neurotrophic factor (GDNF) is a potent neurotrophic factor for dopaminergic neurons. Since dopaminergic neurons degenerate in Parkinson's disease, this factor is a potential therapeutical tool that may save dopaminergic neurons during the pathological process. Moreover, a reduced GDNF expression may be involved in the pathophysiology of the disease. In this study, we tested whether altered GDNF production may participate in the mechanism of cell death in this disease. GDNF gene expression was analyzed by in situ hybridization using riboprobes corresponding to a sequence of the exon 2 human GDNF gene. Experiments were performed on tissue sections of the mesencephalon and the striatum from 8 patients with Parkinson's disease and 6 control subjects matched for age at death and for post mortem delay. No labelling was observed in either group of patients. This absence of detectable expression could not be attributed to methodological problems as a positive staining was observed using the same probes for sections of astroglioma biopsies from human adults and for sections of a newborn infant brain obtained at post-mortem. These data suggest that GDNF is probably expressed at a very low level in the adult human brain and its involvement in the pathophysiology of Parkinson's disease remains to be demonstrated. GDNF may represent a powerful new therapeutic agent for Parkinson's disease, however.
DOI: 10.1007/BF01291789
PubMed: 9013392
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Hunot</name><affiliation wicri:level="3"><nlm:affiliation>INSERM U289, Hôpital de la Salpêtrière, Paris, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>INSERM U289, Hôpital de la Salpêtrière, Paris</wicri:regionArea><placeName><region type="region">Île-de-France</region><region type="old region">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation></author><author><name sortKey="Bernard, V" sort="Bernard, V" uniqKey="Bernard V" first="V" last="Bernard">V. Bernard</name></author><author><name sortKey="Faucheux, B" sort="Faucheux, B" uniqKey="Faucheux B" first="B" last="Faucheux">B. Faucheux</name></author><author><name sortKey="Boissiere, F" sort="Boissiere, F" uniqKey="Boissiere F" first="F" last="Boissière">F. Boissière</name></author><author><name sortKey="Leguern, E" sort="Leguern, E" uniqKey="Leguern E" first="E" last="Leguern">E. Leguern</name></author><author><name sortKey="Brana, C" sort="Brana, C" uniqKey="Brana C" first="C" last="Brana">C. Brana</name></author><author><name sortKey="Gautris, P P" sort="Gautris, P P" uniqKey="Gautris P" first="P P" last="Gautris">P P Gautris</name></author><author><name sortKey="Guerin, J" sort="Guerin, J" uniqKey="Guerin J" first="J" last="Guérin">J. Guérin</name></author><author><name sortKey="Bloch, B" sort="Bloch, B" uniqKey="Bloch B" first="B" last="Bloch">B. Bloch</name></author><author><name sortKey="Agid, Y" sort="Agid, Y" uniqKey="Agid Y" first="Y" last="Agid">Yves Agid</name><affiliation><country>France</country><placeName><settlement type="city">Paris</settlement><region type="region" nuts="2">Île-de-France</region></placeName><orgName type="hospital" n="4">Hôpital de la Salpêtrière</orgName><country>France</country><placeName><settlement type="city">Paris</settlement><region type="region" nuts="2">Île-de-France</region></placeName><orgName type="hospital" n="4">Hôpital de la Salpêtrière</orgName></affiliation></author><author><name sortKey="Hirsch, E C" sort="Hirsch, E C" uniqKey="Hirsch E" first="E C" last="Hirsch">E C Hirsch</name></author></analytic><series><title level="j">Journal of neural transmission (Vienna, Austria : 1996)</title><idno type="ISSN">0300-9564</idno><imprint><date when="1996" type="published">1996</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Brain (metabolism)</term><term>Case-Control Studies</term><term>Cell Death (physiology)</term><term>Gene Expression</term><term>Glial Cell Line-Derived Neurotrophic Factor</term><term>Humans</term><term>In Situ Hybridization</term><term>Nerve Growth Factors (genetics)</term><term>Nerve Tissue Proteins (genetics)</term><term>Parkinson Disease (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Nerve Growth Factors</term><term>Nerve Tissue Proteins</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Glial Cell Line-Derived Neurotrophic Factor</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Brain</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Cell Death</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Case-Control Studies</term><term>Gene Expression</term><term>Humans</term><term>In Situ Hybridization</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Glial cell line-derived neurotrophic factor (GDNF) is a potent neurotrophic factor for dopaminergic neurons. Since dopaminergic neurons degenerate in Parkinson's disease, this factor is a potential therapeutical tool that may save dopaminergic neurons during the pathological process. Moreover, a reduced GDNF expression may be involved in the pathophysiology of the disease. In this study, we tested whether altered GDNF production may participate in the mechanism of cell death in this disease. GDNF gene expression was analyzed by in situ hybridization using riboprobes corresponding to a sequence of the exon 2 human GDNF gene. Experiments were performed on tissue sections of the mesencephalon and the striatum from 8 patients with Parkinson's disease and 6 control subjects matched for age at death and for post mortem delay. No labelling was observed in either group of patients. This absence of detectable expression could not be attributed to methodological problems as a positive staining was observed using the same probes for sections of astroglioma biopsies from human adults and for sections of a newborn infant brain obtained at post-mortem. These data suggest that GDNF is probably expressed at a very low level in the adult human brain and its involvement in the pathophysiology of Parkinson's disease remains to be demonstrated. GDNF may represent a powerful new therapeutic agent for Parkinson's disease, however.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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