CALPAIN INHIBITION PROTECTED SPINAL CORD MOTONEURONS AGAINST 1-METHYL-4-PHENYLPYRIDINIUM ION AND ROTENONE
Identifieur interne : 000361 ( PascalFrancis/Checkpoint ); précédent : 000360; suivant : 000362CALPAIN INHIBITION PROTECTED SPINAL CORD MOTONEURONS AGAINST 1-METHYL-4-PHENYLPYRIDINIUM ION AND ROTENONE
Auteurs : S. Samantaray [États-Unis] ; V. H. Knaryan [États-Unis] ; C. Le Gal [France] ; S. K. Ray [États-Unis] ; N. L. Banik [États-Unis]Source :
- Neuroscience [ 0306-4522 ] ; 2011.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
Parkinson's disease (PD), characterized by selective midbrain nigrostriatal dopaminergic degeneration, is consistently associated with moderate systemic mitochondrial dysfunction. Downstream degeneration of spinal cord has also been suggested in PD, although the mechanisms have not been much investigated. In the present study, two mitochondrial toxicants, 1-methyl-4-phenylpyridinium ion (MPP+) and rotenone were tested in ventral spinal cord (VSC 4.1) motoneuronal cells. Cell death was assessed by morphological and biochemical means to discern a lower apoptosis-inducing concentration and lethal concentration of 50% cell death (LC50), which were subsequently compared in further cytoprotection experiments. Mitochondrial toxicants dose-dependently induced increase in intracellular free Ca2+ level, which was conducive for increased expression and activities of Ca2+-activated neutral protease calpain and downstream caspase-3. Thus, mitochondrial damage triggered apoptotic mechanisms in spinal cord motoneurons. Inhibition of calpain by calpeptin significantly attenuated damaging effects of MPP+ and rotenone on motoneurons, especially at low apoptosis-inducing concentrations of toxicants and partly at their LC50, as demonstrated by absence of DNA ladder formation and decrease in terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL)-positive cells. Cytoprotection by calpeptin was observed with marked decreases in Bax: Bcl-2 ratio and activities of calpain and caspase-3, which affirmed the role of mitochondrial dysfunction and involvement of intrinsic pathway in mediation of apoptosis. These findings strongly suggested that parkinsonian toxicants MPP+ and rotenone at low doses induced cascade of cell-damaging effects in spinal cord motoneurons, thus, highlighting the possibility of induction of apoptotic mechanisms in these cells, when subjected to mitochondrial stress. Cytoprotection rendered by calpeptin further validated the involvement of calpain in apoptosis and suggested calpain inhibition as a potential neuroprotective strategy.
Affiliations:
- France, États-Unis
- Caroline du Sud, Nouvelle-Aquitaine, Poitou-Charentes
- Poitiers
- Université de Poitiers
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en" level="a">CALPAIN INHIBITION PROTECTED SPINAL CORD MOTONEURONS AGAINST 1-METHYL-4-PHENYLPYRIDINIUM ION AND ROTENONE</title><author><name sortKey="Samantaray, S" sort="Samantaray, S" uniqKey="Samantaray S" first="S." last="Samantaray">S. Samantaray</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>Department of Neurosciences, Medical University of South Carolina, 96 Jonathan Lucas Street, Suite 309 CSB, PO Box 250606</s1><s2>Charles-ton, SC 29425</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Caroline du Sud</region></placeName></affiliation></author><author><name sortKey="Knaryan, V H" sort="Knaryan, V H" uniqKey="Knaryan V" first="V. H." last="Knaryan">V. H. Knaryan</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>Department of Neurosciences, Medical University of South Carolina, 96 Jonathan Lucas Street, Suite 309 CSB, PO Box 250606</s1><s2>Charles-ton, SC 29425</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Caroline du Sud</region></placeName></affiliation></author><author><name sortKey="Le Gal, C" sort="Le Gal, C" uniqKey="Le Gal C" first="C." last="Le Gal">C. Le Gal</name><affiliation wicri:level="4"><inist:fA14 i1="02"><s1>Department of Basic and Applied Sciences, Université de Poitiers, 40 Avenue du Recteur Pineau</s1><s2>86022 Poitiers</s2><s3>FRA</s3><sZ>3 aut.</sZ></inist:fA14><country>France</country><placeName><region type="region" nuts="2">Nouvelle-Aquitaine</region><region type="old region" nuts="2">Poitou-Charentes</region><settlement type="city">Poitiers</settlement></placeName><orgName type="university">Université de Poitiers</orgName></affiliation></author><author><name sortKey="Ray, S K" sort="Ray, S K" uniqKey="Ray S" first="S. K." last="Ray">S. K. Ray</name><affiliation wicri:level="2"><inist:fA14 i1="03"><s1>Department of Pathology, Microbiology, and Immunology, University of South Carolina School of Medicine, 6439 Garners Ferry Road</s1><s2>Columbia, SC 29209</s2><s3>USA</s3><sZ>4 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Caroline du Sud</region></placeName></affiliation></author><author><name sortKey="Banik, N L" sort="Banik, N L" uniqKey="Banik N" first="N. L." last="Banik">N. L. Banik</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>Department of Neurosciences, Medical University of South Carolina, 96 Jonathan Lucas Street, Suite 309 CSB, PO Box 250606</s1><s2>Charles-ton, SC 29425</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Caroline du Sud</region></placeName></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">12-0016553</idno><date when="2011">2011</date><idno type="stanalyst">PASCAL 12-0016553 INIST</idno><idno type="RBID">Pascal:12-0016553</idno><idno type="wicri:Area/PascalFrancis/Corpus">000311</idno><idno type="wicri:Area/PascalFrancis/Curation">001010</idno><idno type="wicri:Area/PascalFrancis/Checkpoint">000361</idno><idno type="wicri:explorRef" wicri:stream="PascalFrancis" wicri:step="Checkpoint">000361</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">CALPAIN INHIBITION PROTECTED SPINAL CORD MOTONEURONS AGAINST 1-METHYL-4-PHENYLPYRIDINIUM ION AND ROTENONE</title><author><name sortKey="Samantaray, S" sort="Samantaray, S" uniqKey="Samantaray S" first="S." last="Samantaray">S. Samantaray</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>Department of Neurosciences, Medical University of South Carolina, 96 Jonathan Lucas Street, Suite 309 CSB, PO Box 250606</s1><s2>Charles-ton, SC 29425</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Caroline du Sud</region></placeName></affiliation></author><author><name sortKey="Knaryan, V H" sort="Knaryan, V H" uniqKey="Knaryan V" first="V. H." last="Knaryan">V. H. Knaryan</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>Department of Neurosciences, Medical University of South Carolina, 96 Jonathan Lucas Street, Suite 309 CSB, PO Box 250606</s1><s2>Charles-ton, SC 29425</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Caroline du Sud</region></placeName></affiliation></author><author><name sortKey="Le Gal, C" sort="Le Gal, C" uniqKey="Le Gal C" first="C." last="Le Gal">C. Le Gal</name><affiliation wicri:level="4"><inist:fA14 i1="02"><s1>Department of Basic and Applied Sciences, Université de Poitiers, 40 Avenue du Recteur Pineau</s1><s2>86022 Poitiers</s2><s3>FRA</s3><sZ>3 aut.</sZ></inist:fA14><country>France</country><placeName><region type="region" nuts="2">Nouvelle-Aquitaine</region><region type="old region" nuts="2">Poitou-Charentes</region><settlement type="city">Poitiers</settlement></placeName><orgName type="university">Université de Poitiers</orgName></affiliation></author><author><name sortKey="Ray, S K" sort="Ray, S K" uniqKey="Ray S" first="S. K." last="Ray">S. K. Ray</name><affiliation wicri:level="2"><inist:fA14 i1="03"><s1>Department of Pathology, Microbiology, and Immunology, University of South Carolina School of Medicine, 6439 Garners Ferry Road</s1><s2>Columbia, SC 29209</s2><s3>USA</s3><sZ>4 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Caroline du Sud</region></placeName></affiliation></author><author><name sortKey="Banik, N L" sort="Banik, N L" uniqKey="Banik N" first="N. L." last="Banik">N. L. Banik</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>Department of Neurosciences, Medical University of South Carolina, 96 Jonathan Lucas Street, Suite 309 CSB, PO Box 250606</s1><s2>Charles-ton, SC 29425</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Caroline du Sud</region></placeName></affiliation></author></analytic><series><title level="j" type="main">Neuroscience</title><title level="j" type="abbreviated">Neuroscience</title><idno type="ISSN">0306-4522</idno><imprint><date when="2011">2011</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Neuroscience</title><title level="j" type="abbreviated">Neuroscience</title><idno type="ISSN">0306-4522</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Calpain</term><term>Caspase</term><term>Motor neuron</term><term>Parkinson disease</term><term>Rotenone</term><term>Spinal cord</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Calpain</term><term>Moelle épinière</term><term>Neurone moteur</term><term>Caspase</term><term>Maladie de Parkinson</term><term>Roténone</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease (PD), characterized by selective midbrain nigrostriatal dopaminergic degeneration, is consistently associated with moderate systemic mitochondrial dysfunction. Downstream degeneration of spinal cord has also been suggested in PD, although the mechanisms have not been much investigated. In the present study, two mitochondrial toxicants, 1-methyl-4-phenylpyridinium ion (MPP<sup>+</sup>) and rotenone were tested in ventral spinal cord (VSC 4.1) motoneuronal cells. Cell death was assessed by morphological and biochemical means to discern a lower apoptosis-inducing concentration and lethal concentration of 50% cell death (LC<sub>50</sub>), which were subsequently compared in further cytoprotection experiments. Mitochondrial toxicants dose-dependently induced increase in intracellular free Ca<sup>2+</sup> level, which was conducive for increased expression and activities of Ca<sup>2+</sup>-activated neutral protease calpain and downstream caspase-3. Thus, mitochondrial damage triggered apoptotic mechanisms in spinal cord motoneurons. Inhibition of calpain by calpeptin significantly attenuated damaging effects of MPP<sup>+</sup> and rotenone on motoneurons, especially at low apoptosis-inducing concentrations of toxicants and partly at their LC<sub>50</sub>, as demonstrated by absence of DNA ladder formation and decrease in terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL)-positive cells. Cytoprotection by calpeptin was observed with marked decreases in Bax: Bcl-2 ratio and activities of calpain and caspase-3, which affirmed the role of mitochondrial dysfunction and involvement of intrinsic pathway in mediation of apoptosis. These findings strongly suggested that parkinsonian toxicants MPP<sup>+</sup> and rotenone at low doses induced cascade of cell-damaging effects in spinal cord motoneurons, thus, highlighting the possibility of induction of apoptotic mechanisms in these cells, when subjected to mitochondrial stress. Cytoprotection rendered by calpeptin further validated the involvement of calpain in apoptosis and suggested calpain inhibition as a potential neuroprotective strategy.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0306-4522</s0></fA01><fA02 i1="01"><s0>NRSCDN</s0></fA02><fA03 i2="1"><s0>Neuroscience</s0></fA03><fA05><s2>192</s2></fA05><fA08 i1="01" i2="1" l="ENG"><s1>CALPAIN INHIBITION PROTECTED SPINAL CORD MOTONEURONS AGAINST 1-METHYL-4-PHENYLPYRIDINIUM ION AND ROTENONE</s1></fA08><fA11 i1="01" i2="1"><s1>SAMANTARAY (S.)</s1></fA11><fA11 i1="02" i2="1"><s1>KNARYAN (V. H.)</s1></fA11><fA11 i1="03" i2="1"><s1>LE GAL (C.)</s1></fA11><fA11 i1="04" i2="1"><s1>RAY (S. K.)</s1></fA11><fA11 i1="05" i2="1"><s1>BANIK (N. L.)</s1></fA11><fA14 i1="01"><s1>Department of Neurosciences, Medical University of South Carolina, 96 Jonathan Lucas Street, Suite 309 CSB, PO Box 250606</s1><s2>Charles-ton, SC 29425</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>5 aut.</sZ></fA14><fA14 i1="02"><s1>Department of Basic and Applied Sciences, Université de Poitiers, 40 Avenue du Recteur Pineau</s1><s2>86022 Poitiers</s2><s3>FRA</s3><sZ>3 aut.</sZ></fA14><fA14 i1="03"><s1>Department of Pathology, Microbiology, and Immunology, University of South Carolina School of Medicine, 6439 Garners Ferry Road</s1><s2>Columbia, SC 29209</s2><s3>USA</s3><sZ>4 aut.</sZ></fA14><fA20><s1>263-274</s1></fA20><fA21><s1>2011</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>17194</s2><s5>354000507316380240</s5></fA43><fA44><s0>0000</s0><s1>© 2012 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>2 p.1/4</s0></fA45><fA47 i1="01" i2="1"><s0>12-0016553</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Neuroscience</s0></fA64><fA66 i1="01"><s0>NLD</s0></fA66><fC01 i1="01" l="ENG"><s0>Parkinson's disease (PD), characterized by selective midbrain nigrostriatal dopaminergic degeneration, is consistently associated with moderate systemic mitochondrial dysfunction. Downstream degeneration of spinal cord has also been suggested in PD, although the mechanisms have not been much investigated. In the present study, two mitochondrial toxicants, 1-methyl-4-phenylpyridinium ion (MPP<sup>+</sup>) and rotenone were tested in ventral spinal cord (VSC 4.1) motoneuronal cells. Cell death was assessed by morphological and biochemical means to discern a lower apoptosis-inducing concentration and lethal concentration of 50% cell death (LC<sub>50</sub>), which were subsequently compared in further cytoprotection experiments. Mitochondrial toxicants dose-dependently induced increase in intracellular free Ca<sup>2+</sup> level, which was conducive for increased expression and activities of Ca<sup>2+</sup>-activated neutral protease calpain and downstream caspase-3. Thus, mitochondrial damage triggered apoptotic mechanisms in spinal cord motoneurons. Inhibition of calpain by calpeptin significantly attenuated damaging effects of MPP<sup>+</sup> and rotenone on motoneurons, especially at low apoptosis-inducing concentrations of toxicants and partly at their LC<sub>50</sub>, as demonstrated by absence of DNA ladder formation and decrease in terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL)-positive cells. Cytoprotection by calpeptin was observed with marked decreases in Bax: Bcl-2 ratio and activities of calpain and caspase-3, which affirmed the role of mitochondrial dysfunction and involvement of intrinsic pathway in mediation of apoptosis. These findings strongly suggested that parkinsonian toxicants MPP<sup>+</sup> and rotenone at low doses induced cascade of cell-damaging effects in spinal cord motoneurons, thus, highlighting the possibility of induction of apoptotic mechanisms in these cells, when subjected to mitochondrial stress. 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Samantaray</name></region><name sortKey="Banik, N L" sort="Banik, N L" uniqKey="Banik N" first="N. L." last="Banik">N. L. Banik</name><name sortKey="Knaryan, V H" sort="Knaryan, V H" uniqKey="Knaryan V" first="V. H." last="Knaryan">V. H. Knaryan</name><name sortKey="Ray, S K" sort="Ray, S K" uniqKey="Ray S" first="S. K." last="Ray">S. K. Ray</name></country><country name="France"><region name="Nouvelle-Aquitaine"><name sortKey="Le Gal, C" sort="Le Gal, C" uniqKey="Le Gal C" first="C." last="Le Gal">C. Le Gal</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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