Levodopa activates apoptosis signaling kinase 1 (ASK1) and promotes apoptosis in a neuronal model: implications for the treatment of Parkinson's disease.
Identifieur interne : 000938 ( Main/Exploration ); précédent : 000937; suivant : 000939Levodopa activates apoptosis signaling kinase 1 (ASK1) and promotes apoptosis in a neuronal model: implications for the treatment of Parkinson's disease.
Auteurs : Elizabeth A Sabens Liedhegner [États-Unis] ; Kelly M. Steller ; John J. MieyalSource :
- Chemical research in toxicology [ 1520-5010 ] ; 2011.
Descripteurs français
- KwdFr :
- Anthracènes (pharmacologie), Antienzymes (pharmacologie), Antiparkinsoniens (pharmacologie), Apoptose (effets des médicaments et des substances chimiques), Caspase-3 (métabolisme), Facteur de transcription NF-kappa B (métabolisme), Humains (MeSH), Imidazoles (pharmacologie), JNK Mitogen-Activated Protein Kinases (antagonistes et inhibiteurs), JNK Mitogen-Activated Protein Kinases (biosynthèse), Lignée cellulaire tumorale (MeSH), Lévodopa (pharmacologie), MAP Kinase Kinase Kinase 5 (déficit), MAP Kinase Kinase Kinase 5 (génétique), MAP Kinase Kinase Kinase 5 (métabolisme), Maladie de Parkinson (métabolisme), Neurones dopaminergiques (effets des médicaments et des substances chimiques), Neurones dopaminergiques (métabolisme), Pyridines (pharmacologie), Stress oxydatif (effets des médicaments et des substances chimiques), Survie cellulaire (effets des médicaments et des substances chimiques), Techniques de knock-down de gènes (MeSH), p38 Mitogen-Activated Protein Kinases (antagonistes et inhibiteurs), p38 Mitogen-Activated Protein Kinases (biosynthèse).
- MESH :
- antagonistes et inhibiteurs : JNK Mitogen-Activated Protein Kinases, p38 Mitogen-Activated Protein Kinases.
- biosynthèse : JNK Mitogen-Activated Protein Kinases, p38 Mitogen-Activated Protein Kinases.
- déficit : MAP Kinase Kinase Kinase 5.
- effets des médicaments et des substances chimiques : Apoptose, Neurones dopaminergiques, Stress oxydatif, Survie cellulaire.
- génétique : MAP Kinase Kinase Kinase 5.
- métabolisme : Caspase-3, Facteur de transcription NF-kappa B, MAP Kinase Kinase Kinase 5, Maladie de Parkinson, Neurones dopaminergiques.
- pharmacologie : Anthracènes, Antienzymes, Antiparkinsoniens, Imidazoles, Lévodopa, Pyridines.
- Humains, Lignée cellulaire tumorale, Techniques de knock-down de gènes.
English descriptors
- KwdEn :
- Anthracenes (pharmacology), Antiparkinson Agents (pharmacology), Apoptosis (drug effects), Caspase 3 (metabolism), Cell Line, Tumor (MeSH), Cell Survival (drug effects), Dopaminergic Neurons (drug effects), Dopaminergic Neurons (metabolism), Enzyme Inhibitors (pharmacology), Gene Knockdown Techniques (MeSH), Humans (MeSH), Imidazoles (pharmacology), JNK Mitogen-Activated Protein Kinases (antagonists & inhibitors), JNK Mitogen-Activated Protein Kinases (biosynthesis), Levodopa (pharmacology), MAP Kinase Kinase Kinase 5 (deficiency), MAP Kinase Kinase Kinase 5 (genetics), MAP Kinase Kinase Kinase 5 (metabolism), NF-kappa B (metabolism), Oxidative Stress (drug effects), Parkinson Disease (metabolism), Pyridines (pharmacology), p38 Mitogen-Activated Protein Kinases (antagonists & inhibitors), p38 Mitogen-Activated Protein Kinases (biosynthesis).
- MESH :
- chemical , antagonists & inhibitors : JNK Mitogen-Activated Protein Kinases, p38 Mitogen-Activated Protein Kinases.
- chemical , biosynthesis : JNK Mitogen-Activated Protein Kinases, p38 Mitogen-Activated Protein Kinases.
- chemical , deficiency : MAP Kinase Kinase Kinase 5.
- chemical , genetics : MAP Kinase Kinase Kinase 5.
- chemical , metabolism : Caspase 3, MAP Kinase Kinase Kinase 5, NF-kappa B.
- chemical , pharmacology : Anthracenes, Antiparkinson Agents, Enzyme Inhibitors, Imidazoles, Levodopa, Pyridines.
- drug effects : Apoptosis, Cell Survival, Dopaminergic Neurons, Oxidative Stress.
- metabolism : Dopaminergic Neurons, Parkinson Disease.
- Cell Line, Tumor, Gene Knockdown Techniques, Humans.
Abstract
Oxidative stress is implicated in the etiology of Parkinson's disease (PD), the second most common neurodegenerative disease. PD is treated with chronic administration of l-3,4-dihydroxyphenylalanine (levodopa, L-DOPA), and typically, increasing doses are used during progression of the disease. Paradoxically, L-DOPA is a pro-oxidant and induces cell death in cellular models of PD through disruption of sulfhydryl homeostasis involving loss of the thiol-disulfide oxidoreductase functions of the glutaredoxin (Grx1) and thioredoxin (Trx1) enzyme systems [Sabens, E. A., Distler, A. M., and Mieyal, J. J. (2010) Biochemistry 49 (12), 2715-2724]. Considering this loss of both Grx1 and Trx1 activities upon L-DOPA treatment, we sought to elucidate the mechanism(s) of L-DOPA-induced apoptosis. In other contexts, both the NFκB (nuclear factor κB) pathway and the ASK1 (apoptosis signaling kinase 1) pathway have been shown to be regulated by both Grx1 and Trx1, and both pathways have been implicated in cell death signaling in model systems of PD. Moreover, mixed lineage kinase (MLK) has been considered as a potential therapeutic target for PD. Using SHSY5Y cells as model dopaminergic neurons, we found that NFκB activity was not altered by L-DOPA treatment, and the selective MLK inhibitor (CEP-1347) did not protect the cells from L-DOPA. In contrast, ASK1 was activated with L-DOPA treatment as indicated by phosphorylation of its downstream mitogen-activated protein kinases (MAPK), p38 and JNK. Chemical inhibition of either p38 or JNK provided protection from L-DOPA-induced apoptosis. Moreover, direct knockdown of ASK1 protected from L-DOPA-induced neuronal cell death. These results identify ASK1 as the main pro-apoptotic pathway activated in response to L-DOPA treatment, implicating it as a potential target for adjunct therapy in PD.
DOI: 10.1021/tx200082h
PubMed: 21815648
PubMed Central: PMC3196761
Affiliations:
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cellulaire tumorale (MeSH)</term><term>Lévodopa (pharmacologie)</term><term>MAP Kinase Kinase Kinase 5 (déficit)</term><term>MAP Kinase Kinase Kinase 5 (génétique)</term><term>MAP Kinase Kinase Kinase 5 (métabolisme)</term><term>Maladie de Parkinson (métabolisme)</term><term>Neurones dopaminergiques (effets des médicaments et des substances chimiques)</term><term>Neurones dopaminergiques (métabolisme)</term><term>Pyridines (pharmacologie)</term><term>Stress oxydatif (effets des médicaments et des substances chimiques)</term><term>Survie cellulaire (effets des médicaments et des substances chimiques)</term><term>Techniques de knock-down de gènes (MeSH)</term><term>p38 Mitogen-Activated Protein Kinases (antagonistes et inhibiteurs)</term><term>p38 Mitogen-Activated Protein Kinases (biosynthèse)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>JNK Mitogen-Activated Protein Kinases</term><term>p38 Mitogen-Activated Protein 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Disease</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Caspase-3</term><term>Facteur de transcription NF-kappa B</term><term>MAP Kinase Kinase Kinase 5</term><term>Maladie de Parkinson</term><term>Neurones dopaminergiques</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Anthracènes</term><term>Antienzymes</term><term>Antiparkinsoniens</term><term>Imidazoles</term><term>Lévodopa</term><term>Pyridines</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line, Tumor</term><term>Gene Knockdown Techniques</term><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Techniques de knock-down de gènes</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Oxidative stress is implicated in the etiology of Parkinson's disease (PD), the second most common neurodegenerative disease. PD is treated with chronic administration of l-3,4-dihydroxyphenylalanine (levodopa, L-DOPA), and typically, increasing doses are used during progression of the disease. Paradoxically, L-DOPA is a pro-oxidant and induces cell death in cellular models of PD through disruption of sulfhydryl homeostasis involving loss of the thiol-disulfide oxidoreductase functions of the glutaredoxin (Grx1) and thioredoxin (Trx1) enzyme systems [Sabens, E. A., Distler, A. M., and Mieyal, J. J. (2010) Biochemistry 49 (12), 2715-2724]. Considering this loss of both Grx1 and Trx1 activities upon L-DOPA treatment, we sought to elucidate the mechanism(s) of L-DOPA-induced apoptosis. In other contexts, both the NFκB (nuclear factor κB) pathway and the ASK1 (apoptosis signaling kinase 1) pathway have been shown to be regulated by both Grx1 and Trx1, and both pathways have been implicated in cell death signaling in model systems of PD. Moreover, mixed lineage kinase (MLK) has been considered as a potential therapeutic target for PD. Using SHSY5Y cells as model dopaminergic neurons, we found that NFκB activity was not altered by L-DOPA treatment, and the selective MLK inhibitor (CEP-1347) did not protect the cells from L-DOPA. In contrast, ASK1 was activated with L-DOPA treatment as indicated by phosphorylation of its downstream mitogen-activated protein kinases (MAPK), p38 and JNK. Chemical inhibition of either p38 or JNK provided protection from L-DOPA-induced apoptosis. Moreover, direct knockdown of ASK1 protected from L-DOPA-induced neuronal cell death. These results identify ASK1 as the main pro-apoptotic pathway activated in response to L-DOPA treatment, implicating it as a potential target for adjunct therapy in PD.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">21815648</PMID><DateCompleted><Year>2012</Year><Month>02</Month><Day>27</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1520-5010</ISSN><JournalIssue CitedMedium="Internet"><Volume>24</Volume><Issue>10</Issue><PubDate><Year>2011</Year><Month>Oct</Month><Day>17</Day></PubDate></JournalIssue><Title>Chemical research in toxicology</Title><ISOAbbreviation>Chem Res Toxicol</ISOAbbreviation></Journal><ArticleTitle>Levodopa activates apoptosis signaling kinase 1 (ASK1) and promotes apoptosis in a neuronal model: implications for the treatment of Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>1644-52</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1021/tx200082h</ELocationID><Abstract><AbstractText>Oxidative stress is implicated in the etiology of Parkinson's disease (PD), the second most common neurodegenerative disease. PD is treated with chronic administration of l-3,4-dihydroxyphenylalanine (levodopa, L-DOPA), and typically, increasing doses are used during progression of the disease. Paradoxically, L-DOPA is a pro-oxidant and induces cell death in cellular models of PD through disruption of sulfhydryl homeostasis involving loss of the thiol-disulfide oxidoreductase functions of the glutaredoxin (Grx1) and thioredoxin (Trx1) enzyme systems [Sabens, E. A., Distler, A. M., and Mieyal, J. J. (2010) Biochemistry 49 (12), 2715-2724]. Considering this loss of both Grx1 and Trx1 activities upon L-DOPA treatment, we sought to elucidate the mechanism(s) of L-DOPA-induced apoptosis. In other contexts, both the NFκB (nuclear factor κB) pathway and the ASK1 (apoptosis signaling kinase 1) pathway have been shown to be regulated by both Grx1 and Trx1, and both pathways have been implicated in cell death signaling in model systems of PD. Moreover, mixed lineage kinase (MLK) has been considered as a potential therapeutic target for PD. Using SHSY5Y cells as model dopaminergic neurons, we found that NFκB activity was not altered by L-DOPA treatment, and the selective MLK inhibitor (CEP-1347) did not protect the cells from L-DOPA. In contrast, ASK1 was activated with L-DOPA treatment as indicated by phosphorylation of its downstream mitogen-activated protein kinases (MAPK), p38 and JNK. Chemical inhibition of either p38 or JNK provided protection from L-DOPA-induced apoptosis. Moreover, direct knockdown of ASK1 protected from L-DOPA-induced neuronal cell death. These results identify ASK1 as the main pro-apoptotic pathway activated in response to L-DOPA treatment, implicating it as a potential target for adjunct therapy in PD.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Liedhegner</LastName><ForeName>Elizabeth A Sabens</ForeName><Initials>EA</Initials><AffiliationInfo><Affiliation>Department of Pharmacology, Case Western Reserve University, School of Medicine, 2109 Adelbert Road, Cleveland, OH 44106-4965, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Steller</LastName><ForeName>Kelly M</ForeName><Initials>KM</Initials></Author><Author ValidYN="Y"><LastName>Mieyal</LastName><ForeName>John J</ForeName><Initials>JJ</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>P01 AG015885-04</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P01 AG015885</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32 DK007319-30</GrantID><Acronym>DK</Acronym><Agency>NIDDK NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32 GM008803</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P01 AG 15885</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32 GM008803-08</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32 DK007319</GrantID><Acronym>DK</Acronym><Agency>NIDDK NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>U24 DK076174</GrantID><Acronym>DK</Acronym><Agency>NIDDK NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013486">Research Support, U.S. Gov't, Non-P.H.S.</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2011</Year><Month>08</Month><Day>22</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Chem Res Toxicol</MedlineTA><NlmUniqueID>8807448</NlmUniqueID><ISSNLinking>0893-228X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000873">Anthracenes</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000978">Antiparkinson Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004791">Enzyme Inhibitors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007093">Imidazoles</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016328">NF-kappa B</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011725">Pyridines</NameOfSubstance></Chemical><Chemical><RegistryNumber>1TW30Y2766</RegistryNumber><NameOfSubstance UI="C432165">pyrazolanthrone</NameOfSubstance></Chemical><Chemical><RegistryNumber>46627O600J</RegistryNumber><NameOfSubstance UI="D007980">Levodopa</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.24</RegistryNumber><NameOfSubstance UI="D048031">JNK Mitogen-Activated Protein Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.24</RegistryNumber><NameOfSubstance UI="D048051">p38 Mitogen-Activated Protein Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.25</RegistryNumber><NameOfSubstance UI="D048848">MAP Kinase Kinase Kinase 5</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.25</RegistryNumber><NameOfSubstance UI="C482858">MAP3K5 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.22.-</RegistryNumber><NameOfSubstance UI="D053148">Caspase 3</NameOfSubstance></Chemical><Chemical><RegistryNumber>PVX798P8GI</RegistryNumber><NameOfSubstance UI="C090942">4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazole</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000873" MajorTopicYN="N">Anthracenes</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000978" MajorTopicYN="N">Antiparkinson Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D053148" MajorTopicYN="N">Caspase 3</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045744" MajorTopicYN="N">Cell Line, Tumor</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002470" MajorTopicYN="N">Cell Survival</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D059290" MajorTopicYN="N">Dopaminergic Neurons</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004791" MajorTopicYN="N">Enzyme Inhibitors</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D055785" MajorTopicYN="N">Gene Knockdown 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