RapamycinFungusV1, Main, Exploration, bibRecord, 000604

FOXO protects against age-progressive axonal degeneration.

Identifieur interne : 000604 ( Main/Exploration ); précédent : 000603; suivant : 000605

FOXO protects against age-progressive axonal degeneration.

Auteurs : Inah Hwang [États-Unis] ; Hwanhee Oh [États-Unis] ; Evan Santo [États-Unis] ; Do-Yeon Kim [Corée du Sud] ; John W. Chen [États-Unis] ; Roderick T. Bronson [États-Unis] ; Jason W. Locasale [États-Unis] ; Yoonmi Na [États-Unis] ; Jaclyn Lee [États-Unis] ; Stewart Reed [États-Unis] ; Miklos Toth [États-Unis] ; Wai H. Yu [États-Unis] ; Florian L. Muller [États-Unis] ; Jihye Paik [États-Unis]

Source :

Aging cell [ 1474-9726 ] ; 2018.

RBID : pubmed:29178390

Descripteurs français

KwdFr :
- Agents protecteurs (métabolisme), Agents protecteurs (pharmacologie), Animaux (MeSH), Axones (métabolisme), Complexe-1 cible mécanistique de la rapamycine (métabolisme), Facteurs de transcription Forkhead (génétique), Facteurs de transcription Forkhead (métabolisme), Régulation de l'expression des gènes (physiologie), Souris knockout (MeSH), Transduction du signal (MeSH), Vieillissement (métabolisme).
MESH :
- génétique : Facteurs de transcription Forkhead.
- métabolisme : Agents protecteurs, Axones, Complexe-1 cible mécanistique de la rapamycine, Facteurs de transcription Forkhead, Vieillissement.
- pharmacologie : Agents protecteurs.
- physiologie : Régulation de l'expression des gènes.
- Animaux, Souris knockout, Transduction du signal.

English descriptors

KwdEn :
- Aging (metabolism), Animals (MeSH), Axons (metabolism), Forkhead Transcription Factors (genetics), Forkhead Transcription Factors (metabolism), Gene Expression Regulation (physiology), Mechanistic Target of Rapamycin Complex 1 (metabolism), Mice, Knockout (MeSH), Protective Agents (metabolism), Protective Agents (pharmacology), Signal Transduction (MeSH).
MESH :
- chemical , genetics : Forkhead Transcription Factors.
- metabolism : Aging, Axons, Forkhead Transcription Factors, Mechanistic Target of Rapamycin Complex 1, Protective Agents.
- chemical , pharmacology : Protective Agents.
- physiology : Gene Expression Regulation.
- Animals, Mice, Knockout, Signal Transduction.

Abstract

Neurodegeneration resulting in cognitive and motor impairment is an inevitable consequence of aging. Little is known about the genetic regulation of this process despite its overriding importance in normal aging. Here, we identify the Forkhead Box O (FOXO) transcription factor 1, 3, and 4 isoforms as a guardian of neuronal integrity by inhibiting age-progressive axonal degeneration in mammals. FOXO expression progressively increased in aging human and mouse brains. The nervous system-specific deletion of Foxo transcription factors in mice accelerates aging-related axonal tract degeneration, which is followed by motor dysfunction. This accelerated neurodegeneration is accompanied by levels of white matter astrogliosis and microgliosis in middle-aged Foxo knockout mice that are typically only observed in very old wild-type mice and other aged mammals, including humans. Mechanistically, axonal degeneration in nerve-specific Foxo knockout mice is associated with elevated mTORC1 activity and accompanying proteotoxic stress due to decreased Sestrin3 expression. Inhibition of mTORC1 by rapamycin treatment mimics FOXO action and prevented axonal degeneration in Foxo knockout mice with accelerated nervous system aging. Defining this central role for FOXO in neuroprotection during mammalian aging offers an invaluable window into the aging process itself.

DOI: 10.1111/acel.12701
PubMed: 29178390
PubMed Central: PMC5771393

Affiliations:

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000666
to stream Main, to step Curation: 000666

Le document en format XML

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<author><name sortKey="Lee, Jaclyn" sort="Lee, Jaclyn" uniqKey="Lee J" first="Jaclyn" last="Lee">Jaclyn Lee</name>
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<wicri:regionArea>Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA</wicri:regionArea>
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<author><name sortKey="Muller, Florian L" sort="Muller, Florian L" uniqKey="Muller F" first="Florian L" last="Muller">Florian L. Muller</name>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aging (metabolism)</term>
<term>Animals (MeSH)</term>
<term>Axons (metabolism)</term>
<term>Forkhead Transcription Factors (genetics)</term>
<term>Forkhead Transcription Factors (metabolism)</term>
<term>Gene Expression Regulation (physiology)</term>
<term>Mechanistic Target of Rapamycin Complex 1 (metabolism)</term>
<term>Mice, Knockout (MeSH)</term>
<term>Protective Agents (metabolism)</term>
<term>Protective Agents (pharmacology)</term>
<term>Signal Transduction (MeSH)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Agents protecteurs (métabolisme)</term>
<term>Agents protecteurs (pharmacologie)</term>
<term>Animaux (MeSH)</term>
<term>Axones (métabolisme)</term>
<term>Complexe-1 cible mécanistique de la rapamycine (métabolisme)</term>
<term>Facteurs de transcription Forkhead (génétique)</term>
<term>Facteurs de transcription Forkhead (métabolisme)</term>
<term>Régulation de l'expression des gènes (physiologie)</term>
<term>Souris knockout (MeSH)</term>
<term>Transduction du signal (MeSH)</term>
<term>Vieillissement (métabolisme)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Forkhead Transcription Factors</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Facteurs de transcription Forkhead</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Aging</term>
<term>Axons</term>
<term>Forkhead Transcription Factors</term>
<term>Mechanistic Target of Rapamycin Complex 1</term>
<term>Protective Agents</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Agents protecteurs</term>
<term>Axones</term>
<term>Complexe-1 cible mécanistique de la rapamycine</term>
<term>Facteurs de transcription Forkhead</term>
<term>Vieillissement</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Agents protecteurs</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Protective Agents</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Régulation de l'expression des gènes</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Gene Expression Regulation</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Mice, Knockout</term>
<term>Signal Transduction</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Souris knockout</term>
<term>Transduction du signal</term>
</keywords>
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<front><div type="abstract" xml:lang="en">Neurodegeneration resulting in cognitive and motor impairment is an inevitable consequence of aging. Little is known about the genetic regulation of this process despite its overriding importance in normal aging. Here, we identify the Forkhead Box O (FOXO) transcription factor 1, 3, and 4 isoforms as a guardian of neuronal integrity by inhibiting age-progressive axonal degeneration in mammals. FOXO expression progressively increased in aging human and mouse brains. The nervous system-specific deletion of Foxo transcription factors in mice accelerates aging-related axonal tract degeneration, which is followed by motor dysfunction. This accelerated neurodegeneration is accompanied by levels of white matter astrogliosis and microgliosis in middle-aged Foxo knockout mice that are typically only observed in very old wild-type mice and other aged mammals, including humans. Mechanistically, axonal degeneration in nerve-specific Foxo knockout mice is associated with elevated mTORC1 activity and accompanying proteotoxic stress due to decreased Sestrin3 expression. Inhibition of mTORC1 by rapamycin treatment mimics FOXO action and prevented axonal degeneration in Foxo knockout mice with accelerated nervous system aging. Defining this central role for FOXO in neuroprotection during mammalian aging offers an invaluable window into the aging process itself.</div>
</front>
</TEI>
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<DateCompleted><Year>2019</Year>
<Month>07</Month>
<Day>30</Day>
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<Title>Aging cell</Title>
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<ArticleTitle>FOXO protects against age-progressive axonal degeneration.</ArticleTitle>
<ELocationID EIdType="doi" ValidYN="Y">10.1111/acel.12701</ELocationID>
<Abstract><AbstractText>Neurodegeneration resulting in cognitive and motor impairment is an inevitable consequence of aging. Little is known about the genetic regulation of this process despite its overriding importance in normal aging. Here, we identify the Forkhead Box O (FOXO) transcription factor 1, 3, and 4 isoforms as a guardian of neuronal integrity by inhibiting age-progressive axonal degeneration in mammals. FOXO expression progressively increased in aging human and mouse brains. The nervous system-specific deletion of Foxo transcription factors in mice accelerates aging-related axonal tract degeneration, which is followed by motor dysfunction. This accelerated neurodegeneration is accompanied by levels of white matter astrogliosis and microgliosis in middle-aged Foxo knockout mice that are typically only observed in very old wild-type mice and other aged mammals, including humans. Mechanistically, axonal degeneration in nerve-specific Foxo knockout mice is associated with elevated mTORC1 activity and accompanying proteotoxic stress due to decreased Sestrin3 expression. Inhibition of mTORC1 by rapamycin treatment mimics FOXO action and prevented axonal degeneration in Foxo knockout mice with accelerated nervous system aging. Defining this central role for FOXO in neuroprotection during mammalian aging offers an invaluable window into the aging process itself.</AbstractText>
<CopyrightInformation>© 2017 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hwang</LastName>
<ForeName>Inah</ForeName>
<Initials>I</Initials>
<AffiliationInfo><Affiliation>Department of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, NY, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Oh</LastName>
<ForeName>Hwanhee</ForeName>
<Initials>H</Initials>
<AffiliationInfo><Affiliation>Department of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, NY, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Santo</LastName>
<ForeName>Evan</ForeName>
<Initials>E</Initials>
<AffiliationInfo><Affiliation>Department of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, NY, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kim</LastName>
<ForeName>Do-Yeon</ForeName>
<Initials>DY</Initials>
<AffiliationInfo><Affiliation>Department of Pharmacology, School of Dentistry, Kyungpook National University, Daegu, Korea.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chen</LastName>
<ForeName>John W</ForeName>
<Initials>JW</Initials>
<AffiliationInfo><Affiliation>Center for Systems Biology and the Division of Neuroradiology, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Bronson</LastName>
<ForeName>Roderick T</ForeName>
<Initials>RT</Initials>
<AffiliationInfo><Affiliation>Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Locasale</LastName>
<ForeName>Jason W</ForeName>
<Initials>JW</Initials>
<AffiliationInfo><Affiliation>Department of Pharmacology and Cancer Biology, Duke University School of Medicine, Durham, NC, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Na</LastName>
<ForeName>Yoonmi</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Department of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, NY, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lee</LastName>
<ForeName>Jaclyn</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Reed</LastName>
<ForeName>Stewart</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Toth</LastName>
<ForeName>Miklos</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Pharmacology, Weill Cornell Medicine, New York, NY, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Yu</LastName>
<ForeName>Wai H</ForeName>
<Initials>WH</Initials>
<AffiliationInfo><Affiliation>Department of Pathology and Cell Biology, Columbia University, New York, NY, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Muller</LastName>
<ForeName>Florian L</ForeName>
<Initials>FL</Initials>
<AffiliationInfo><Affiliation>Cancer Systems Imaging, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Paik</LastName>
<ForeName>Jihye</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, NY, USA.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>R01 CA193256</GrantID>
<Acronym>CA</Acronym>
<Agency>NCI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 AG048284</GrantID>
<Acronym>AG</Acronym>
<Agency>NIA NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R56 AG048284</GrantID>
<Acronym>AG</Acronym>
<Agency>NIA NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R00 CA168997</GrantID>
<Acronym>CA</Acronym>
<Agency>NCI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>P30 DK020541</GrantID>
<Acronym>DK</Acronym>
<Agency>NIDDK NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>S10 OD018164</GrantID>
<Acronym>OD</Acronym>
<Agency>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="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2017</Year>
<Month>11</Month>
<Day>26</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>England</Country>
<MedlineTA>Aging Cell</MedlineTA>
<NlmUniqueID>101130839</NlmUniqueID>
<ISSNLinking>1474-9718</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D051858">Forkhead Transcription Factors</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D020011">Protective Agents</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber>
<NameOfSubstance UI="D000076222">Mechanistic Target of Rapamycin Complex 1</NameOfSubstance>
</Chemical>
</ChemicalList>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000375" MajorTopicYN="N">Aging</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001369" MajorTopicYN="N">Axons</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051858" MajorTopicYN="N">Forkhead Transcription Factors</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005786" MajorTopicYN="N">Gene Expression Regulation</DescriptorName>
<QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000076222" MajorTopicYN="N">Mechanistic Target of Rapamycin Complex 1</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D020011" MajorTopicYN="N">Protective Agents</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">FOXO
</Keyword>
<Keyword MajorTopicYN="Y">accelerated aging</Keyword>
<Keyword MajorTopicYN="Y">aging</Keyword>
<Keyword MajorTopicYN="Y">central nervous system</Keyword>
<Keyword MajorTopicYN="Y">mouse models</Keyword>
<Keyword MajorTopicYN="Y">neurodegeneration</Keyword>
<Keyword MajorTopicYN="Y">neuroinflammation</Keyword>
<Keyword MajorTopicYN="Y">oxidative stress</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="accepted"><Year>2017</Year>
<Month>10</Month>
<Day>08</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed"><Year>2017</Year>
<Month>11</Month>
<Day>28</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2019</Year>
<Month>7</Month>
<Day>31</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2017</Year>
<Month>11</Month>
<Day>28</Day>
<Hour>6</Hour>
<Minute>0</Minute>
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<PublicationStatus>ppublish</PublicationStatus>
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<affiliations><list><country><li>Corée du Sud</li>
<li>États-Unis</li>
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<li>Massachusetts</li>
<li>Texas</li>
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	Serveur d'exploration sur la rapamycine et les champignons
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FOXO protects against age-progressive axonal degeneration.

FOXO protects against age-progressive axonal degeneration.

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