Estradiol and tamoxifen differentially regulate a plasmalemmal voltage-dependent anion channel involved in amyloid-beta induced neurotoxicity.
Identifieur interne : 000815 ( Ncbi/Merge ); précédent : 000814; suivant : 000816Estradiol and tamoxifen differentially regulate a plasmalemmal voltage-dependent anion channel involved in amyloid-beta induced neurotoxicity.
Auteurs : Jose Luis Herrera [Espagne] ; Cecilia Fernandez ; Mario Diaz ; Debora Cury ; Raquel MarinSource :
- Steroids [ 1878-5867 ] ; 2011.
Descripteurs français
- KwdFr :
- Animaux, Canaux anioniques voltage-dépendants (métabolisme), Humains, Maladie d'Alzheimer (métabolisme), Maladie d'Alzheimer (traitement médicamenteux), Microdomaines membranaires (métabolisme), Modulateurs sélectifs des récepteurs des oestrogènes (pharmacologie), Modulateurs sélectifs des récepteurs des oestrogènes (usage thérapeutique), Neuroprotecteurs (usage thérapeutique), Oestradiol (métabolisme), Oestradiol (physiologie), Oestradiol (usage thérapeutique), Oestrogènes (métabolisme), Oestrogènes (physiologie), Oestrogènes (usage thérapeutique), Peptides bêta-amyloïdes (métabolisme), Phosphorylation, Protein Phosphatase 2 (métabolisme), Tamoxifène (pharmacologie), Tamoxifène (usage thérapeutique), Transduction du signal.
- MESH :
- métabolisme : Canaux anioniques voltage-dépendants, Maladie d'Alzheimer, Microdomaines membranaires, Oestradiol, Oestrogènes, Peptides bêta-amyloïdes, Protein Phosphatase 2.
- pharmacologie : Modulateurs sélectifs des récepteurs des oestrogènes, Tamoxifène.
- physiologie : Oestradiol, Oestrogènes.
- traitement médicamenteux : Maladie d'Alzheimer.
- usage thérapeutique : Modulateurs sélectifs des récepteurs des oestrogènes, Neuroprotecteurs, Oestradiol, Oestrogènes, Tamoxifène.
- Animaux, Humains, Phosphorylation, Transduction du signal.
English descriptors
- KwdEn :
- Alzheimer Disease (drug therapy), Alzheimer Disease (metabolism), Amyloid beta-Peptides (metabolism), Animals, Estradiol (metabolism), Estradiol (physiology), Estradiol (therapeutic use), Estrogens (metabolism), Estrogens (physiology), Estrogens (therapeutic use), Humans, Membrane Microdomains (metabolism), Neuroprotective Agents (therapeutic use), Phosphorylation, Protein Phosphatase 2 (metabolism), Selective Estrogen Receptor Modulators (pharmacology), Selective Estrogen Receptor Modulators (therapeutic use), Signal Transduction, Tamoxifen (pharmacology), Tamoxifen (therapeutic use), Voltage-Dependent Anion Channels (metabolism).
- MESH :
- chemical , metabolism : Amyloid beta-Peptides, Estradiol, Estrogens, Protein Phosphatase 2, Voltage-Dependent Anion Channels.
- drug therapy : Alzheimer Disease.
- metabolism : Alzheimer Disease, Membrane Microdomains.
- chemical , pharmacology : Selective Estrogen Receptor Modulators, Tamoxifen.
- chemical , physiology : Estradiol, Estrogens.
- chemical , therapeutic use : Estradiol, Estrogens, Neuroprotective Agents, Selective Estrogen Receptor Modulators, Tamoxifen.
- Animals, Humans, Phosphorylation, Signal Transduction.
Abstract
There is a wealth of information indicating that estradiol exerts rapid actions involved in neuroprotection and cognitive-enhancing effects. Some of these effects appear to delay onset, or even ameliorate, the neuropathology of Alzheimer's disease (AD), although some controversy exists about the beneficial brain effects of estrogen therapies. Therefore, it is crucial to better understand the mechanisms developed by 17β-estradiol to signal in the brain. At the neuronal membrane, the hormone can rapidly interact with estrogen receptors (mERs) or activate other receptors, such as G protein-coupled and ionotropic receptors. And the list of membrane signalling molecules modulated by estradiol in neurons is increasing. VDAC is a voltage-dependent anion channel, known as a mitochondrial porin which is also found at the neuronal membrane, where it appears to be involved in redox regulation, extrinsic apoptosis and amyloid beta neurotoxicity. Moreover, VDAC is present in neuronal lipid rafts, where it is associated with estrogen receptor α-like (mER), forming part of a macromolecular complex together with caveolin-1 and other signalling proteins related to neuronal preservation. Interestingly, we have recently found that 17β-estradiol rapidly promotes VDAC phosphorylation through the activation of protein kinase A (PKA) and Src-kinase, which may be relevant to maintain this channel inactivated. On the contrary, tamoxifen, a selective estrogen receptor modulator (SERM), provokes the dephosphorylation of VDAC, and eventually its opening, by activating a cascade of phosphatases, including protein phosphatase 2 (PP2A). This review will focus on the relevance of these novel findings in the alternative estrogen mechanisms to achieve neuroprotection related to AD.
DOI: 10.1016/j.steroids.2011.02.014
PubMed: 21354436
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pubmed:21354436Le document en format XML
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Modulators</term><term>Tamoxifen</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Oestradiol</term><term>Oestrogènes</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Estradiol</term><term>Estrogens</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Estradiol</term><term>Estrogens</term><term>Neuroprotective Agents</term><term>Selective Estrogen Receptor Modulators</term><term>Tamoxifen</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Maladie d'Alzheimer</term></keywords><keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr"><term>Modulateurs sélectifs des récepteurs des oestrogènes</term><term>Neuroprotecteurs</term><term>Oestradiol</term><term>Oestrogènes</term><term>Tamoxifène</term></keywords><keywords scheme="MESH" 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Moreover, VDAC is present in neuronal lipid rafts, where it is associated with estrogen receptor α-like (mER), forming part of a macromolecular complex together with caveolin-1 and other signalling proteins related to neuronal preservation. Interestingly, we have recently found that 17β-estradiol rapidly promotes VDAC phosphorylation through the activation of protein kinase A (PKA) and Src-kinase, which may be relevant to maintain this channel inactivated. On the contrary, tamoxifen, a selective estrogen receptor modulator (SERM), provokes the dephosphorylation of VDAC, and eventually its opening, by activating a cascade of phosphatases, including protein phosphatase 2 (PP2A). This review will focus on the relevance of these novel findings in the alternative estrogen mechanisms to achieve neuroprotection related to AD.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">21354436</PMID><DateCompleted><Year>2011</Year><Month>10</Month><Day>25</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1878-5867</ISSN><JournalIssue CitedMedium="Internet"><Volume>76</Volume><Issue>9</Issue><PubDate><Year>2011</Year><Month>Aug</Month></PubDate></JournalIssue><Title>Steroids</Title><ISOAbbreviation>Steroids</ISOAbbreviation></Journal><ArticleTitle>Estradiol and tamoxifen differentially regulate a plasmalemmal voltage-dependent anion channel involved in amyloid-beta induced neurotoxicity.</ArticleTitle><Pagination><MedlinePgn>840-4</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.steroids.2011.02.014</ELocationID><Abstract><AbstractText>There is a wealth of information indicating that estradiol exerts rapid actions involved in neuroprotection and cognitive-enhancing effects. Some of these effects appear to delay onset, or even ameliorate, the neuropathology of Alzheimer's disease (AD), although some controversy exists about the beneficial brain effects of estrogen therapies. Therefore, it is crucial to better understand the mechanisms developed by 17β-estradiol to signal in the brain. At the neuronal membrane, the hormone can rapidly interact with estrogen receptors (mERs) or activate other receptors, such as G protein-coupled and ionotropic receptors. And the list of membrane signalling molecules modulated by estradiol in neurons is increasing. VDAC is a voltage-dependent anion channel, known as a mitochondrial porin which is also found at the neuronal membrane, where it appears to be involved in redox regulation, extrinsic apoptosis and amyloid beta neurotoxicity. Moreover, VDAC is present in neuronal lipid rafts, where it is associated with estrogen receptor α-like (mER), forming part of a macromolecular complex together with caveolin-1 and other signalling proteins related to neuronal preservation. Interestingly, we have recently found that 17β-estradiol rapidly promotes VDAC phosphorylation through the activation of protein kinase A (PKA) and Src-kinase, which may be relevant to maintain this channel inactivated. On the contrary, tamoxifen, a selective estrogen receptor modulator (SERM), provokes the dephosphorylation of VDAC, and eventually its opening, by activating a cascade of phosphatases, including protein phosphatase 2 (PP2A). This review will focus on the relevance of these novel findings in the alternative estrogen mechanisms to achieve neuroprotection related to AD.</AbstractText><CopyrightInformation>Copyright © 2011 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Herrera</LastName><ForeName>Jose Luis</ForeName><Initials>JL</Initials><AffiliationInfo><Affiliation>Laboratory of Cellular Neurobiology, Department of Physiology & Institute of Biomedical Technologies, University of La Laguna, School of Medicine, Santa Cruz de Tenerife, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fernandez</LastName><ForeName>Cecilia</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Diaz</LastName><ForeName>Mario</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Cury</LastName><ForeName>Debora</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Marin</LastName><ForeName>Raquel</ForeName><Initials>R</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2011</Year><Month>02</Month><Day>25</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Steroids</MedlineTA><NlmUniqueID>0404536</NlmUniqueID><ISSNLinking>0039-128X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016229">Amyloid beta-Peptides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004967">Estrogens</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018696">Neuroprotective Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D020845">Selective Estrogen Receptor Modulators</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance 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sortKey="Herrera, Jose Luis" sort="Herrera, Jose Luis" uniqKey="Herrera J" first="Jose Luis" last="Herrera">Jose Luis Herrera</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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