The Deleterious Effects of Oxidative and Nitrosative Stress on Palmitoylation, Membrane Lipid Rafts and Lipid-Based Cellular Signalling: New Drug Targets in Neuroimmune Disorders.
Identifieur interne : 001644 ( Main/Exploration ); précédent : 001643; suivant : 001645The Deleterious Effects of Oxidative and Nitrosative Stress on Palmitoylation, Membrane Lipid Rafts and Lipid-Based Cellular Signalling: New Drug Targets in Neuroimmune Disorders.
Auteurs : Gerwyn Morris [Royaume-Uni] ; Ken Walder [Australie] ; Basant K. Puri [Royaume-Uni] ; Michael Berk [Australie] ; Michael Maes [Australie, Thaïlande, Brésil]Source :
- Molecular neurobiology [ 1559-1182 ] ; 2016.
Descripteurs français
- KwdFr :
- Acides gras omega-3 (administration et posologie), Animaux (MeSH), Humains (MeSH), Lipoylation (effets des médicaments et des substances chimiques), Lipoylation (physiologie), Maladies du système nerveux (immunologie), Maladies du système nerveux (métabolisme), Maladies du système nerveux (traitement médicamenteux), Membrane cellulaire (effets des médicaments et des substances chimiques), Membrane cellulaire (immunologie), Membrane cellulaire (métabolisme), Microdomaines membranaires (effets des médicaments et des substances chimiques), Microdomaines membranaires (immunologie), Microdomaines membranaires (métabolisme), Neuro-immunomodulation (effets des médicaments et des substances chimiques), Neuro-immunomodulation (physiologie), Oxydoréduction (MeSH), Stress nitrosatif (effets des médicaments et des substances chimiques), Stress nitrosatif (physiologie), Stress oxydatif (effets des médicaments et des substances chimiques), Stress oxydatif (physiologie), Systèmes de délivrance de médicaments (tendances), Transduction du signal (effets des médicaments et des substances chimiques), Transduction du signal (physiologie).
- MESH :
- administration et posologie : Acides gras omega-3.
- effets des médicaments et des substances chimiques : Lipoylation, Membrane cellulaire, Microdomaines membranaires, Neuro-immunomodulation, Stress nitrosatif, Stress oxydatif, Transduction du signal.
- immunologie : Maladies du système nerveux, Membrane cellulaire, Microdomaines membranaires.
- métabolisme : Maladies du système nerveux, Membrane cellulaire, Microdomaines membranaires.
- physiologie : Lipoylation, Neuro-immunomodulation, Stress nitrosatif, Stress oxydatif, Transduction du signal.
- tendances : Systèmes de délivrance de médicaments.
- traitement médicamenteux : Maladies du système nerveux.
- Animaux, Humains, Oxydoréduction.
English descriptors
- KwdEn :
- Animals (MeSH), Cell Membrane (drug effects), Cell Membrane (immunology), Cell Membrane (metabolism), Drug Delivery Systems (trends), Fatty Acids, Omega-3 (administration & dosage), Humans (MeSH), Lipoylation (drug effects), Lipoylation (physiology), Membrane Microdomains (drug effects), Membrane Microdomains (immunology), Membrane Microdomains (metabolism), Nervous System Diseases (drug therapy), Nervous System Diseases (immunology), Nervous System Diseases (metabolism), Neuroimmunomodulation (drug effects), Neuroimmunomodulation (physiology), Nitrosative Stress (drug effects), Nitrosative Stress (physiology), Oxidation-Reduction (MeSH), Oxidative Stress (drug effects), Oxidative Stress (physiology), Signal Transduction (drug effects), Signal Transduction (physiology).
- MESH :
- chemical , administration & dosage : Fatty Acids, Omega-3.
- drug effects : Cell Membrane, Lipoylation, Membrane Microdomains, Neuroimmunomodulation, Nitrosative Stress, Oxidative Stress, Signal Transduction.
- drug therapy : Nervous System Diseases.
- immunology : Cell Membrane, Membrane Microdomains, Nervous System Diseases.
- metabolism : Cell Membrane, Membrane Microdomains, Nervous System Diseases.
- physiology : Lipoylation, Neuroimmunomodulation, Nitrosative Stress, Oxidative Stress, Signal Transduction.
- trends : Drug Delivery Systems.
- Animals, Humans, Oxidation-Reduction.
Abstract
Oxidative and nitrosative stress (O&NS) is causatively implicated in the pathogenesis of Alzheimer's and Parkinson's disease, multiple sclerosis, chronic fatigue syndrome, schizophrenia and depression. Many of the consequences stemming from O&NS, including damage to proteins, lipids and DNA, are well known, whereas the effects of O&NS on lipoprotein-based cellular signalling involving palmitoylation and plasma membrane lipid rafts are less well documented. The aim of this narrative review is to discuss the mechanisms involved in lipid-based signalling, including palmitoylation, membrane/lipid raft (MLR) and n-3 polyunsaturated fatty acid (PUFA) functions, the effects of O&NS processes on these processes and their role in the abovementioned diseases. S-palmitoylation is a post-translational modification, which regulates protein trafficking and association with the plasma membrane, protein subcellular location and functions. Palmitoylation and MRLs play a key role in neuronal functions, including glutamatergic neurotransmission, and immune-inflammatory responses. Palmitoylation, MLRs and n-3 PUFAs are vulnerable to the corruptive effects of O&NS. Chronic O&NS inhibits palmitoylation and causes profound changes in lipid membrane composition, e.g. n-3 PUFA depletion, increased membrane permeability and reduced fluidity, which together lead to disorders in intracellular signal transduction, receptor dysfunction and increased neurotoxicity. Disruption of lipid-based signalling is a source of the neuroimmune disorders involved in the pathophysiology of the abovementioned diseases. n-3 PUFA supplementation is a rational therapeutic approach targeting disruptions in lipid-based signalling.
DOI: 10.1007/s12035-015-9392-y
PubMed: 26310971
Affiliations:
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Puri</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medicine, Hammersmith Hospital, Imperial College London, London, W12 0HS, UK.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Department of Medicine, Hammersmith Hospital, Imperial College London, London, W12 0HS</wicri:regionArea><wicri:noRegion>W12 0HS</wicri:noRegion></affiliation></author><author><name sortKey="Berk, Michael" sort="Berk, Michael" uniqKey="Berk M" first="Michael" last="Berk">Michael Berk</name><affiliation wicri:level="1"><nlm:affiliation>Orygen, The National Centre of Excellence in Youth Mental Health and the Centre of Youth Mental Health, Poplar Road 35, Parkville, 3052, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Orygen, The National Centre of Excellence in Youth Mental Health and the Centre of Youth Mental Health, Poplar Road 35, Parkville, 3052</wicri:regionArea><wicri:noRegion>3052</wicri:noRegion></affiliation><affiliation wicri:level="4"><nlm:affiliation>The Florey Institute for Neuroscience and Mental Health, University of Melbourne, Kenneth Myer Building, Royal Parade 30, Parkville, 3052, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>The Florey Institute for Neuroscience and Mental Health, University of Melbourne, Kenneth Myer Building, Royal Parade 30, Parkville, 3052</wicri:regionArea><orgName type="university">Université de Melbourne</orgName><placeName><settlement type="city">Melbourne</settlement><region type="état">Victoria (État)</region></placeName></affiliation><affiliation wicri:level="4"><nlm:affiliation>Department of Psychiatry, Royal Melbourne Hospital, University of Melbourne, Level 1 North, Main Block, Parkville, 3052, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Department of Psychiatry, Royal Melbourne Hospital, University of Melbourne, Level 1 North, Main Block, Parkville, 3052</wicri:regionArea><orgName type="university">Université de Melbourne</orgName><placeName><settlement type="city">Melbourne</settlement><region type="état">Victoria (État)</region></placeName></affiliation><affiliation wicri:level="1"><nlm:affiliation>IMPACT Strategic Research Center, School of Medicine, Deakin University, P.O. 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Box 291, Geelong, 3220</wicri:regionArea><wicri:noRegion>3220</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:affiliation>Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand. dr.michaelmaes@hotmail.com.</nlm:affiliation><country xml:lang="fr">Thaïlande</country><wicri:regionArea>Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok</wicri:regionArea><wicri:noRegion>Bangkok</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:affiliation>Health Sciences Graduate Program, Health Sciences Center, State University of Londrina, Londrina, Brazil. dr.michaelmaes@hotmail.com.</nlm:affiliation><country xml:lang="fr">Brésil</country><wicri:regionArea>Health Sciences Graduate Program, Health Sciences Center, State University of Londrina, Londrina</wicri:regionArea><wicri:noRegion>Londrina</wicri:noRegion></affiliation></author></analytic><series><title level="j">Molecular neurobiology</title><idno type="eISSN">1559-1182</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Cell Membrane (drug effects)</term><term>Cell Membrane (immunology)</term><term>Cell Membrane (metabolism)</term><term>Drug Delivery Systems (trends)</term><term>Fatty Acids, Omega-3 (administration & dosage)</term><term>Humans (MeSH)</term><term>Lipoylation (drug effects)</term><term>Lipoylation (physiology)</term><term>Membrane Microdomains (drug effects)</term><term>Membrane Microdomains (immunology)</term><term>Membrane Microdomains (metabolism)</term><term>Nervous System Diseases (drug therapy)</term><term>Nervous System Diseases (immunology)</term><term>Nervous System Diseases (metabolism)</term><term>Neuroimmunomodulation (drug effects)</term><term>Neuroimmunomodulation (physiology)</term><term>Nitrosative Stress (drug effects)</term><term>Nitrosative Stress (physiology)</term><term>Oxidation-Reduction (MeSH)</term><term>Oxidative Stress (drug effects)</term><term>Oxidative Stress (physiology)</term><term>Signal Transduction (drug effects)</term><term>Signal Transduction (physiology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Acides gras omega-3 (administration et posologie)</term><term>Animaux (MeSH)</term><term>Humains (MeSH)</term><term>Lipoylation (effets des médicaments et des substances chimiques)</term><term>Lipoylation (physiologie)</term><term>Maladies du système nerveux (immunologie)</term><term>Maladies du système nerveux (métabolisme)</term><term>Maladies du système nerveux (traitement médicamenteux)</term><term>Membrane cellulaire (effets des médicaments et des substances chimiques)</term><term>Membrane cellulaire (immunologie)</term><term>Membrane cellulaire (métabolisme)</term><term>Microdomaines membranaires (effets des médicaments et des substances chimiques)</term><term>Microdomaines membranaires (immunologie)</term><term>Microdomaines membranaires (métabolisme)</term><term>Neuro-immunomodulation (effets des médicaments et des substances chimiques)</term><term>Neuro-immunomodulation (physiologie)</term><term>Oxydoréduction (MeSH)</term><term>Stress nitrosatif (effets des médicaments et des substances chimiques)</term><term>Stress nitrosatif (physiologie)</term><term>Stress oxydatif (effets des médicaments et des substances chimiques)</term><term>Stress oxydatif (physiologie)</term><term>Systèmes de délivrance de médicaments (tendances)</term><term>Transduction du signal (effets des médicaments et des substances chimiques)</term><term>Transduction du signal (physiologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Fatty Acids, Omega-3</term></keywords><keywords scheme="MESH" qualifier="administration et posologie" xml:lang="fr"><term>Acides gras omega-3</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Membrane</term><term>Lipoylation</term><term>Membrane Microdomains</term><term>Neuroimmunomodulation</term><term>Nitrosative Stress</term><term>Oxidative Stress</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Nervous System Diseases</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Lipoylation</term><term>Membrane cellulaire</term><term>Microdomaines membranaires</term><term>Neuro-immunomodulation</term><term>Stress nitrosatif</term><term>Stress oxydatif</term><term>Transduction du signal</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Maladies du système nerveux</term><term>Membrane cellulaire</term><term>Microdomaines membranaires</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Cell Membrane</term><term>Membrane Microdomains</term><term>Nervous System Diseases</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Cell Membrane</term><term>Membrane Microdomains</term><term>Nervous System Diseases</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Maladies du système nerveux</term><term>Membrane cellulaire</term><term>Microdomaines membranaires</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Lipoylation</term><term>Neuro-immunomodulation</term><term>Stress nitrosatif</term><term>Stress oxydatif</term><term>Transduction du signal</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Lipoylation</term><term>Neuroimmunomodulation</term><term>Nitrosative Stress</term><term>Oxidative Stress</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="tendances" xml:lang="fr"><term>Systèmes de délivrance de médicaments</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Maladies du système nerveux</term></keywords><keywords scheme="MESH" qualifier="trends" xml:lang="en"><term>Drug Delivery Systems</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Humans</term><term>Oxidation-Reduction</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Humains</term><term>Oxydoréduction</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Oxidative and nitrosative stress (O&NS) is causatively implicated in the pathogenesis of Alzheimer's and Parkinson's disease, multiple sclerosis, chronic fatigue syndrome, schizophrenia and depression. Many of the consequences stemming from O&NS, including damage to proteins, lipids and DNA, are well known, whereas the effects of O&NS on lipoprotein-based cellular signalling involving palmitoylation and plasma membrane lipid rafts are less well documented. The aim of this narrative review is to discuss the mechanisms involved in lipid-based signalling, including palmitoylation, membrane/lipid raft (MLR) and n-3 polyunsaturated fatty acid (PUFA) functions, the effects of O&NS processes on these processes and their role in the abovementioned diseases. S-palmitoylation is a post-translational modification, which regulates protein trafficking and association with the plasma membrane, protein subcellular location and functions. Palmitoylation and MRLs play a key role in neuronal functions, including glutamatergic neurotransmission, and immune-inflammatory responses. Palmitoylation, MLRs and n-3 PUFAs are vulnerable to the corruptive effects of O&NS. Chronic O&NS inhibits palmitoylation and causes profound changes in lipid membrane composition, e.g. n-3 PUFA depletion, increased membrane permeability and reduced fluidity, which together lead to disorders in intracellular signal transduction, receptor dysfunction and increased neurotoxicity. Disruption of lipid-based signalling is a source of the neuroimmune disorders involved in the pathophysiology of the abovementioned diseases. n-3 PUFA supplementation is a rational therapeutic approach targeting disruptions in lipid-based signalling.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26310971</PMID><DateCompleted><Year>2018</Year><Month>01</Month><Day>16</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1559-1182</ISSN><JournalIssue CitedMedium="Internet"><Volume>53</Volume><Issue>7</Issue><PubDate><Year>2016</Year><Month>09</Month></PubDate></JournalIssue><Title>Molecular neurobiology</Title><ISOAbbreviation>Mol Neurobiol</ISOAbbreviation></Journal><ArticleTitle>The Deleterious Effects of Oxidative and Nitrosative Stress on Palmitoylation, Membrane Lipid Rafts and Lipid-Based Cellular Signalling: New Drug Targets in Neuroimmune Disorders.</ArticleTitle><Pagination><MedlinePgn>4638-58</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s12035-015-9392-y</ELocationID><Abstract><AbstractText>Oxidative and nitrosative stress (O&NS) is causatively implicated in the pathogenesis of Alzheimer's and Parkinson's disease, multiple sclerosis, chronic fatigue syndrome, schizophrenia and depression. Many of the consequences stemming from O&NS, including damage to proteins, lipids and DNA, are well known, whereas the effects of O&NS on lipoprotein-based cellular signalling involving palmitoylation and plasma membrane lipid rafts are less well documented. The aim of this narrative review is to discuss the mechanisms involved in lipid-based signalling, including palmitoylation, membrane/lipid raft (MLR) and n-3 polyunsaturated fatty acid (PUFA) functions, the effects of O&NS processes on these processes and their role in the abovementioned diseases. S-palmitoylation is a post-translational modification, which regulates protein trafficking and association with the plasma membrane, protein subcellular location and functions. Palmitoylation and MRLs play a key role in neuronal functions, including glutamatergic neurotransmission, and immune-inflammatory responses. Palmitoylation, MLRs and n-3 PUFAs are vulnerable to the corruptive effects of O&NS. Chronic O&NS inhibits palmitoylation and causes profound changes in lipid membrane composition, e.g. n-3 PUFA depletion, increased membrane permeability and reduced fluidity, which together lead to disorders in intracellular signal transduction, receptor dysfunction and increased neurotoxicity. Disruption of lipid-based signalling is a source of the neuroimmune disorders involved in the pathophysiology of the abovementioned diseases. n-3 PUFA supplementation is a rational therapeutic approach targeting disruptions in lipid-based signalling.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Morris</LastName><ForeName>Gerwyn</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Tir Na Nog, Bryn Road seaside 87, Llanelli, SA152LW, Wales, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Walder</LastName><ForeName>Ken</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Metabolic Research Unit, Deakin University, Geelong, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Puri</LastName><ForeName>Basant K</ForeName><Initials>BK</Initials><AffiliationInfo><Affiliation>Department of Medicine, Hammersmith Hospital, Imperial College London, London, W12 0HS, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Berk</LastName><ForeName>Michael</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Orygen, The National Centre of Excellence in Youth Mental Health and the Centre of Youth Mental Health, Poplar Road 35, Parkville, 3052, Australia.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>The Florey Institute for Neuroscience and Mental Health, University of Melbourne, Kenneth Myer Building, Royal Parade 30, Parkville, 3052, Australia.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Psychiatry, Royal Melbourne Hospital, University of Melbourne, Level 1 North, Main Block, Parkville, 3052, Australia.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>IMPACT Strategic Research Center, School of Medicine, Deakin University, P.O. Box 291, Geelong, 3220, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Maes</LastName><ForeName>Michael</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>IMPACT Strategic Research Center, School of Medicine, Deakin University, P.O. Box 291, Geelong, 3220, Australia. dr.michaelmaes@hotmail.com.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand. dr.michaelmaes@hotmail.com.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Health Sciences Graduate Program, Health Sciences Center, State University of Londrina, Londrina, Brazil. dr.michaelmaes@hotmail.com.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>08</Month><Day>27</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mol 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uniqKey="Morris G" first="Gerwyn" last="Morris">Gerwyn Morris</name></noRegion><name sortKey="Puri, Basant K" sort="Puri, Basant K" uniqKey="Puri B" first="Basant K" last="Puri">Basant K. Puri</name></country><country name="Australie"><noRegion><name sortKey="Walder, Ken" sort="Walder, Ken" uniqKey="Walder K" first="Ken" last="Walder">Ken Walder</name></noRegion><name sortKey="Berk, Michael" sort="Berk, Michael" uniqKey="Berk M" first="Michael" last="Berk">Michael Berk</name><name sortKey="Berk, Michael" sort="Berk, Michael" uniqKey="Berk M" first="Michael" last="Berk">Michael Berk</name><name sortKey="Berk, Michael" sort="Berk, Michael" uniqKey="Berk M" first="Michael" last="Berk">Michael Berk</name><name sortKey="Berk, Michael" sort="Berk, Michael" uniqKey="Berk M" first="Michael" last="Berk">Michael Berk</name><name sortKey="Maes, Michael" sort="Maes, Michael" uniqKey="Maes M" first="Michael" last="Maes">Michael Maes</name></country><country name="Thaïlande"><noRegion><name sortKey="Maes, Michael" sort="Maes, Michael" uniqKey="Maes M" first="Michael" last="Maes">Michael Maes</name></noRegion></country><country name="Brésil"><noRegion><name sortKey="Maes, Michael" sort="Maes, Michael" uniqKey="Maes M" first="Michael" last="Maes">Michael Maes</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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