Morphological and molecular characterization of the response of differentiated PC12 cells to calcium stress.
Identifieur interne : 001C99 ( Ncbi/Curation ); précédent : 001C98; suivant : 001D00Morphological and molecular characterization of the response of differentiated PC12 cells to calcium stress.
Auteurs : P P Michel [France] ; S. Vyas ; P. Anglade ; M. Ruberg ; Yves Agid [France]Source :
- The European journal of neuroscience [ 0953-816X ] ; 1994.
English descriptors
- KwdEn :
- Animals, Apoptosis, Calcimycin (pharmacology), Calcium (metabolism), Cell Differentiation (physiology), Cell Survival, Cycloheximide (pharmacology), DNA (metabolism), DNA Damage, Dopamine (metabolism), Dose-Response Relationship, Drug, Humans, Microscopy, Electron, Models, Neurological, Neurites (drug effects), Neurites (physiology), Neurites (ultrastructure), Neurons (drug effects), Neurons (metabolism), Neurons (ultrastructure), PC12 Cells, Parkinson Disease, Tyrosine 3-Monooxygenase (biosynthesis).
- MESH :
- chemical , biosynthesis : Tyrosine 3-Monooxygenase.
- chemical , metabolism : Calcium, DNA, Dopamine.
- chemical , pharmacology : Calcimycin, Cycloheximide.
- drug effects : Neurites, Neurons.
- metabolism : Neurons.
- physiology : Cell Differentiation, Neurites.
- ultrastructure : Neurites, Neurons.
- Animals, Apoptosis, Cell Survival, DNA Damage, Dose-Response Relationship, Drug, Humans, Microscopy, Electron, Models, Neurological, PC12 Cells, Parkinson Disease.
Abstract
The mechanisms that lead ultimately to neuronal death in pathological ageing of the brain remain mostly unknown as in the case of Parkinson's disease where there is a progressive and selective loss of dopaminergic neurons within the substantia nigra. Dopamine-expressing PC12 cells that were neuronally differentiated by nerve growth factor treatment were chosen as a culture model in which to study some of the changes that may occur during the course of the degenerative process. They were exposed to the calcium ionophore A23187 in order to produce a sustained rise in cytoplasmic calcium, a phenomenon related to various pathological conditions. The degenerative effects of the ionophore were dose- and time-dependent. They were characterized by early fragmentation of the neurites followed ultimately by a loss in cell viability. Biochemical changes, such as a decrease in [3H]dopamine uptake and modulations of the tyrosine hydroxylase gene, were detected before macroscopic evidence of cell suffering (e.g. neurite fragmentation) could be observed. Although an ongoing degenerative process was occurring in cell somata, PC12 cells were able to recover upon ionophore withdrawal. Characteristics of apoptosis such as chromatin condensation and DNA fragmentation were detectable in a small population of dying cells. DNA fragmentation could be prevented by the endonuclease inhibitor aurintricarboxylic acid. New protein synthesis was not required, as cycloheximide failed to prevent degeneration. Taken together, these results suggest that differentiated PC12 cells react to calcium stress through a sequence of regulatory processes which appears to be independent of the apoptotic pathway.
PubMed: 7912984
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Anglade</name></author><author><name sortKey="Ruberg, M" sort="Ruberg, M" uniqKey="Ruberg M" first="M" last="Ruberg">M. Ruberg</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></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1994">1994</date><idno type="RBID">pubmed:7912984</idno><idno type="pmid">7912984</idno><idno type="wicri:Area/PubMed/Corpus">001686</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001686</idno><idno type="wicri:Area/PubMed/Curation">001645</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">001645</idno><idno type="wicri:Area/PubMed/Checkpoint">001645</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">001645</idno><idno type="wicri:Area/Ncbi/Merge">001C99</idno><idno type="wicri:Area/Ncbi/Curation">001C99</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Morphological and molecular characterization of the response of differentiated PC12 cells to calcium stress.</title><author><name sortKey="Michel, P P" sort="Michel, P P" uniqKey="Michel P" first="P P" last="Michel">P P Michel</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="Vyas, S" sort="Vyas, S" uniqKey="Vyas S" first="S" last="Vyas">S. Vyas</name></author><author><name sortKey="Anglade, P" sort="Anglade, P" uniqKey="Anglade P" first="P" last="Anglade">P. Anglade</name></author><author><name sortKey="Ruberg, M" sort="Ruberg, M" uniqKey="Ruberg M" first="M" last="Ruberg">M. Ruberg</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></analytic><series><title level="j">The European journal of neuroscience</title><idno type="ISSN">0953-816X</idno><imprint><date when="1994" type="published">1994</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Apoptosis</term><term>Calcimycin (pharmacology)</term><term>Calcium (metabolism)</term><term>Cell Differentiation (physiology)</term><term>Cell Survival</term><term>Cycloheximide (pharmacology)</term><term>DNA (metabolism)</term><term>DNA Damage</term><term>Dopamine (metabolism)</term><term>Dose-Response Relationship, Drug</term><term>Humans</term><term>Microscopy, Electron</term><term>Models, Neurological</term><term>Neurites (drug effects)</term><term>Neurites (physiology)</term><term>Neurites (ultrastructure)</term><term>Neurons (drug effects)</term><term>Neurons (metabolism)</term><term>Neurons (ultrastructure)</term><term>PC12 Cells</term><term>Parkinson Disease</term><term>Tyrosine 3-Monooxygenase (biosynthesis)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Tyrosine 3-Monooxygenase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Calcium</term><term>DNA</term><term>Dopamine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Calcimycin</term><term>Cycloheximide</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Neurites</term><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Cell Differentiation</term><term>Neurites</term></keywords><keywords scheme="MESH" qualifier="ultrastructure" xml:lang="en"><term>Neurites</term><term>Neurons</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Apoptosis</term><term>Cell Survival</term><term>DNA Damage</term><term>Dose-Response Relationship, Drug</term><term>Humans</term><term>Microscopy, Electron</term><term>Models, Neurological</term><term>PC12 Cells</term><term>Parkinson Disease</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The mechanisms that lead ultimately to neuronal death in pathological ageing of the brain remain mostly unknown as in the case of Parkinson's disease where there is a progressive and selective loss of dopaminergic neurons within the substantia nigra. Dopamine-expressing PC12 cells that were neuronally differentiated by nerve growth factor treatment were chosen as a culture model in which to study some of the changes that may occur during the course of the degenerative process. They were exposed to the calcium ionophore A23187 in order to produce a sustained rise in cytoplasmic calcium, a phenomenon related to various pathological conditions. The degenerative effects of the ionophore were dose- and time-dependent. They were characterized by early fragmentation of the neurites followed ultimately by a loss in cell viability. Biochemical changes, such as a decrease in [3H]dopamine uptake and modulations of the tyrosine hydroxylase gene, were detected before macroscopic evidence of cell suffering (e.g. neurite fragmentation) could be observed. Although an ongoing degenerative process was occurring in cell somata, PC12 cells were able to recover upon ionophore withdrawal. Characteristics of apoptosis such as chromatin condensation and DNA fragmentation were detectable in a small population of dying cells. DNA fragmentation could be prevented by the endonuclease inhibitor aurintricarboxylic acid. New protein synthesis was not required, as cycloheximide failed to prevent degeneration. Taken together, these results suggest that differentiated PC12 cells react to calcium stress through a sequence of regulatory processes which appears to be independent of the apoptotic pathway.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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