Erythropoietin is neuroprotective in a transgenic mouse model of multiple system atrophy.
Identifieur interne : 001334 ( PubMed/Curation ); précédent : 001333; suivant : 001335Erythropoietin is neuroprotective in a transgenic mouse model of multiple system atrophy.
Auteurs : Martin Köllensperger [Autriche] ; Florian Krismer ; Anton Pallua ; Nadia Stefanova ; Werner Poewe ; Gregor K. WenningSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2011.
English descriptors
- KwdEn :
- Animals, Cell Death (drug effects), Convulsants (toxicity), Corpus Striatum (pathology), Disease Models, Animal, Dopamine and cAMP-Regulated Phosphoprotein 32 (metabolism), Drug Administration Schedule, Erythropoietin (therapeutic use), Exploratory Behavior (drug effects), Humans, Mice, Mice, Transgenic, Motor Activity (drug effects), Multiple System Atrophy (drug therapy), Multiple System Atrophy (genetics), Multiple System Atrophy (physiopathology), Myelin Proteolipid Protein (genetics), Nitro Compounds (toxicity), Propionates (toxicity), Substantia Nigra (pathology), Tyrosine 3-Monooxygenase (metabolism), alpha-Synuclein (genetics).
- MESH :
- chemical , genetics : Myelin Proteolipid Protein, alpha-Synuclein.
- chemical , metabolism : Dopamine and cAMP-Regulated Phosphoprotein 32, Tyrosine 3-Monooxygenase.
- chemical , therapeutic use : Erythropoietin.
- chemical , toxicity : Convulsants, Nitro Compounds, Propionates.
- drug effects : Cell Death, Exploratory Behavior, Motor Activity.
- drug therapy : Multiple System Atrophy.
- genetics : Multiple System Atrophy.
- pathology : Corpus Striatum, Substantia Nigra.
- physiopathology : Multiple System Atrophy.
- Animals, Disease Models, Animal, Drug Administration Schedule, Humans, Mice, Mice, Transgenic.
Abstract
Multiple system atrophy is a rapidly progressive neurodegenerative disorder with a markedly reduced life expectancy. Failure of symptomatic treatment raises an urgent need for disease-modifying strategies. We have investigated the neuroprotective potential of erythropoietin in (proteolipid protein)-α-synuclein transgenic mice exposed to 3-nitropropionic acid featuring multiple system atrophy-like pathology including oligodendroglial α-synuclein inclusions and selective neuronal degeneration. Mice were treated with erythropoietin starting before (early erythropoietin) and after (late erythropoietin) intoxication with 3-nitropropionic acid. Nonintoxicated animals receiving erythropoietin and intoxicated animals treated with saline served as control groups. Behavioral tests included pole test, open field activity, and motor behavior scale. Immunohistochemistry for tyrosine hydroxylase and dopamine and cyclic adenosine monophosphate-regulated phosphoprotein (DARPP-32) was analyzed stereologically. Animals receiving erythropoietin before and after 3-nitropropionic acid intoxication scored significantly lower on the motor behavior scale and they performed better in the pole test than controls with no significant difference between early and late erythropoietin administration. Similarly, rearing scores were worse in 3-nitropropionic acid-treated animals with no difference between the erythropoietin subgroups. Immunohistochemistry revealed significant attenuation of 3-nitropropionic acid-induced loss of tyrosine hydroxylase and DARPP-32 positive neurons in substantia nigra pars compacta and striatum, respectively, in both erythropoietin-treated groups without significant group difference in the substantia nigra. However, at striatal level, a significant difference between early and late erythropoietin administration was observed. In the combined (proteolipid protein)-α-synuclein 3-nitropropionic acid multiple system atrophy mouse model, erythropoietin appears to rescue dopaminergic and striatal gabaergic projection neurons. This effect is associated with improved motor function. Further studies are warranted to develop erythropoietin as a potential interventional therapy in multiple system atrophy.
DOI: 10.1002/mds.23474
PubMed: 21462262
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Wenning</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2011" type="published">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Cell Death (drug effects)</term><term>Convulsants (toxicity)</term><term>Corpus Striatum (pathology)</term><term>Disease Models, Animal</term><term>Dopamine and cAMP-Regulated Phosphoprotein 32 (metabolism)</term><term>Drug Administration Schedule</term><term>Erythropoietin (therapeutic use)</term><term>Exploratory Behavior (drug effects)</term><term>Humans</term><term>Mice</term><term>Mice, Transgenic</term><term>Motor Activity (drug effects)</term><term>Multiple System Atrophy (drug therapy)</term><term>Multiple System Atrophy (genetics)</term><term>Multiple System Atrophy (physiopathology)</term><term>Myelin Proteolipid Protein (genetics)</term><term>Nitro Compounds (toxicity)</term><term>Propionates (toxicity)</term><term>Substantia Nigra (pathology)</term><term>Tyrosine 3-Monooxygenase (metabolism)</term><term>alpha-Synuclein (genetics)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Myelin Proteolipid Protein</term><term>alpha-Synuclein</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine and cAMP-Regulated Phosphoprotein 32</term><term>Tyrosine 3-Monooxygenase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Erythropoietin</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Convulsants</term><term>Nitro Compounds</term><term>Propionates</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Death</term><term>Exploratory Behavior</term><term>Motor Activity</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Multiple System Atrophy</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Multiple System Atrophy</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Corpus Striatum</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Multiple System Atrophy</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Drug Administration Schedule</term><term>Humans</term><term>Mice</term><term>Mice, Transgenic</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Multiple system atrophy is a rapidly progressive neurodegenerative disorder with a markedly reduced life expectancy. Failure of symptomatic treatment raises an urgent need for disease-modifying strategies. We have investigated the neuroprotective potential of erythropoietin in (proteolipid protein)-α-synuclein transgenic mice exposed to 3-nitropropionic acid featuring multiple system atrophy-like pathology including oligodendroglial α-synuclein inclusions and selective neuronal degeneration. Mice were treated with erythropoietin starting before (early erythropoietin) and after (late erythropoietin) intoxication with 3-nitropropionic acid. Nonintoxicated animals receiving erythropoietin and intoxicated animals treated with saline served as control groups. Behavioral tests included pole test, open field activity, and motor behavior scale. Immunohistochemistry for tyrosine hydroxylase and dopamine and cyclic adenosine monophosphate-regulated phosphoprotein (DARPP-32) was analyzed stereologically. Animals receiving erythropoietin before and after 3-nitropropionic acid intoxication scored significantly lower on the motor behavior scale and they performed better in the pole test than controls with no significant difference between early and late erythropoietin administration. Similarly, rearing scores were worse in 3-nitropropionic acid-treated animals with no difference between the erythropoietin subgroups. Immunohistochemistry revealed significant attenuation of 3-nitropropionic acid-induced loss of tyrosine hydroxylase and DARPP-32 positive neurons in substantia nigra pars compacta and striatum, respectively, in both erythropoietin-treated groups without significant group difference in the substantia nigra. However, at striatal level, a significant difference between early and late erythropoietin administration was observed. In the combined (proteolipid protein)-α-synuclein 3-nitropropionic acid multiple system atrophy mouse model, erythropoietin appears to rescue dopaminergic and striatal gabaergic projection neurons. This effect is associated with improved motor function. Further studies are warranted to develop erythropoietin as a potential interventional therapy in multiple system atrophy.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">21462262</PMID><DateCreated><Year>2011</Year><Month>04</Month><Day>04</Day></DateCreated><DateCompleted><Year>2011</Year><Month>07</Month><Day>29</Day></DateCompleted><DateRevised><Year>2012</Year><Month>11</Month><Day>15</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>26</Volume><Issue>3</Issue><PubDate><Year>2011</Year><Month>Feb</Month><Day>15</Day></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Erythropoietin is neuroprotective in a transgenic mouse model of multiple system atrophy.</ArticleTitle><Pagination><MedlinePgn>507-15</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.23474</ELocationID><Abstract><AbstractText>Multiple system atrophy is a rapidly progressive neurodegenerative disorder with a markedly reduced life expectancy. Failure of symptomatic treatment raises an urgent need for disease-modifying strategies. We have investigated the neuroprotective potential of erythropoietin in (proteolipid protein)-α-synuclein transgenic mice exposed to 3-nitropropionic acid featuring multiple system atrophy-like pathology including oligodendroglial α-synuclein inclusions and selective neuronal degeneration. Mice were treated with erythropoietin starting before (early erythropoietin) and after (late erythropoietin) intoxication with 3-nitropropionic acid. Nonintoxicated animals receiving erythropoietin and intoxicated animals treated with saline served as control groups. Behavioral tests included pole test, open field activity, and motor behavior scale. Immunohistochemistry for tyrosine hydroxylase and dopamine and cyclic adenosine monophosphate-regulated phosphoprotein (DARPP-32) was analyzed stereologically. Animals receiving erythropoietin before and after 3-nitropropionic acid intoxication scored significantly lower on the motor behavior scale and they performed better in the pole test than controls with no significant difference between early and late erythropoietin administration. Similarly, rearing scores were worse in 3-nitropropionic acid-treated animals with no difference between the erythropoietin subgroups. Immunohistochemistry revealed significant attenuation of 3-nitropropionic acid-induced loss of tyrosine hydroxylase and DARPP-32 positive neurons in substantia nigra pars compacta and striatum, respectively, in both erythropoietin-treated groups without significant group difference in the substantia nigra. However, at striatal level, a significant difference between early and late erythropoietin administration was observed. In the combined (proteolipid protein)-α-synuclein 3-nitropropionic acid multiple system atrophy mouse model, erythropoietin appears to rescue dopaminergic and striatal gabaergic projection neurons. This effect is associated with improved motor function. Further studies are warranted to develop erythropoietin as a potential interventional therapy in multiple system atrophy.</AbstractText><CopyrightInformation>Copyright © 2011 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Köllensperger</LastName><ForeName>Martin</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Division of Clinical Neurobiology, Department of Neurology, Medical University, Innsbruck, Austria. martin.koellensperger@gmail.com</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Krismer</LastName><ForeName>Florian</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Pallua</LastName><ForeName>Anton</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Stefanova</LastName><ForeName>Nadia</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Poewe</LastName><ForeName>Werner</ForeName><Initials>W</Initials></Author><Author ValidYN="Y"><LastName>Wenning</LastName><ForeName>Gregor K</ForeName><Initials>GK</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2011</Year><Month>01</Month><Day>06</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D003292">Convulsants</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051937">Dopamine and cAMP-Regulated Phosphoprotein 32</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018991">Myelin Proteolipid Protein</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009574">Nitro Compounds</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011422">Propionates</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051844">alpha-Synuclein</NameOfSubstance></Chemical><Chemical><RegistryNumber>11096-26-7</RegistryNumber><NameOfSubstance UI="D004921">Erythropoietin</NameOfSubstance></Chemical><Chemical><RegistryNumber>504-88-1</RegistryNumber><NameOfSubstance UI="C015392">3-nitropropionic acid</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.16.2</RegistryNumber><NameOfSubstance UI="D014446">Tyrosine 3-Monooxygenase</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000818">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" 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UI="D004921">Erythropoietin</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000627">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005106">Exploratory Behavior</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D051379">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008822">Mice, Transgenic</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009043">Motor Activity</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D019578">Multiple System Atrophy</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000188">drug therapy</QualifierName><QualifierName MajorTopicYN="Y" 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UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D051844">alpha-Synuclein</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2009</Year><Month>12</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2010</Year><Month>6</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2010</Year><Month>9</Month><Day>13</Day></PubMedPubDate><PubMedPubDate PubStatus="aheadofprint"><Year>2011</Year><Month>1</Month><Day>6</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2011</Year><Month>4</Month><Day>5</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2011</Year><Month>4</Month><Day>5</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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