Autophagy alteration prevents primary cilium disassembly in RPE1 cells.
Identifieur interne : 000656 ( Main/Exploration ); précédent : 000655; suivant : 000657Autophagy alteration prevents primary cilium disassembly in RPE1 cells.
Auteurs : Yunash Maharjan [Corée du Sud] ; Joon No Lee [Corée du Sud] ; Seongae Kwak [Corée du Sud] ; Hyewon Lim [Corée du Sud] ; Raghbendra Kumar Dutta [Corée du Sud] ; Zhi-Qiang Liu [Corée du Sud] ; Hong-Seob So [Corée du Sud] ; Raekil Park [Corée du Sud]Source :
- Biochemical and biophysical research communications [ 1090-2104 ] ; 2018.
Descripteurs français
- KwdFr :
- Autophagie (effets des médicaments et des substances chimiques), Cils vibratiles (effets des médicaments et des substances chimiques), Cils vibratiles (métabolisme), Humains (MeSH), Lignée cellulaire (MeSH), Sirolimus (pharmacologie), Sérum (métabolisme), Épithélium pigmentaire de la rétine (cytologie).
- MESH :
- cytologie : Épithélium pigmentaire de la rétine.
- effets des médicaments et des substances chimiques : Autophagie, Cils vibratiles.
- métabolisme : Cils vibratiles, Sérum.
- pharmacologie : Sirolimus.
- Humains, Lignée cellulaire.
English descriptors
- KwdEn :
- MESH :
Abstract
Primary cilium is a microtubule structure that emanates from the surface of most human cells. Primary cilia assemble during the resting stage (G0 phase) and disassemble with cell cycle progression. Defects associated with the control of the assembly or disassembly of the primary cilium have been implicated in various human diseases, including ciliopathy and cancer. Although studies have suggested the interplay between activation of autophagy and ciliogenesis, any direct mechanism between autophagy abatement and disassembly of primary cilium remains elusive. In this study, we found that the gradual abatement in autophagy during serum-restimulation was a dynamic process and significantly correlated with the disassembly of primary cilium in human retinal pigmented epithelial (RPE1) cells. Although autophagy activity was gradually decreased during serum-restimulation, the alteration in autophagy under the same condition prevented the disassembly of the primary cilium. Autophagy inhibitors such as chloroquine, U18666A and 3-methyladenine (3-MA) retained both the number of ciliated cells and cilium length. In contrast, rapamycin treatment during serum-restimulation maintained the number of ciliated cells with shortened cilia. Taken together, alteration in autophagy during serum-restimulation prevent the disassembly of the primary cilium, and autophagy modulators may serve as useful compounds for studying mechanistic details related to the disassembly of the primary cilium and ciliopathy.
DOI: 10.1016/j.bbrc.2018.04.051
PubMed: 29649478
Affiliations:
Links toward previous steps (curation, corpus...)
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Center for Metabolic Function Regulation, Wonkwang University, School of Medicine, Iksan, Jeonbuk, 54538, South Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Microbiology, Wonkwang University, School of Medicine, Iksan, Jeonbuk, 54538, South Korea; Center for Metabolic Function Regulation, Wonkwang University, School of Medicine, Iksan, Jeonbuk, 54538</wicri:regionArea><wicri:noRegion>54538</wicri:noRegion></affiliation></author><author><name sortKey="Lee, Joon No" sort="Lee, Joon No" uniqKey="Lee J" first="Joon No" last="Lee">Joon No Lee</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biomedical Science & Engineering, GIST Research Institute, Gwangju Institute of Science & Technology, Gwangju, 61005, South Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Biomedical Science & Engineering, GIST Research Institute, Gwangju Institute of Science & Technology, Gwangju, 61005</wicri:regionArea><wicri:noRegion>61005</wicri:noRegion></affiliation></author><author><name sortKey="Kwak, Seongae" sort="Kwak, Seongae" uniqKey="Kwak S" first="Seongae" last="Kwak">Seongae Kwak</name><affiliation wicri:level="1"><nlm:affiliation>Zoonosis Research Center, Wonkwang University School of Medicine, Iksan, Jeonbuk, 54538, South Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Zoonosis Research Center, Wonkwang University School of Medicine, Iksan, Jeonbuk, 54538</wicri:regionArea><wicri:noRegion>54538</wicri:noRegion></affiliation></author><author><name sortKey="Lim, Hyewon" sort="Lim, Hyewon" uniqKey="Lim H" first="Hyewon" last="Lim">Hyewon Lim</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology, Wonkwang University, School of Medicine, Iksan, Jeonbuk, 54538, South Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Microbiology, Wonkwang University, School of Medicine, Iksan, Jeonbuk, 54538</wicri:regionArea><wicri:noRegion>54538</wicri:noRegion></affiliation></author><author><name sortKey="Dutta, Raghbendra Kumar" sort="Dutta, Raghbendra Kumar" uniqKey="Dutta R" first="Raghbendra Kumar" last="Dutta">Raghbendra Kumar Dutta</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology, Wonkwang University, School of Medicine, Iksan, Jeonbuk, 54538, South Korea; Center for Metabolic Function Regulation, Wonkwang University, School of Medicine, Iksan, Jeonbuk, 54538, South Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Microbiology, Wonkwang University, School of Medicine, Iksan, Jeonbuk, 54538, South Korea; Center for Metabolic Function Regulation, Wonkwang University, School of Medicine, Iksan, Jeonbuk, 54538</wicri:regionArea><wicri:noRegion>54538</wicri:noRegion></affiliation></author><author><name sortKey="Liu, Zhi Qiang" sort="Liu, Zhi Qiang" uniqKey="Liu Z" first="Zhi-Qiang" last="Liu">Zhi-Qiang Liu</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology, Wonkwang University, School of Medicine, Iksan, Jeonbuk, 54538, South Korea; Center for Metabolic Function Regulation, Wonkwang University, School of Medicine, Iksan, Jeonbuk, 54538, South Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Microbiology, Wonkwang University, School of Medicine, Iksan, Jeonbuk, 54538, South Korea; Center for Metabolic Function Regulation, Wonkwang University, School of Medicine, Iksan, Jeonbuk, 54538</wicri:regionArea><wicri:noRegion>54538</wicri:noRegion></affiliation></author><author><name sortKey="So, Hong Seob" sort="So, Hong Seob" uniqKey="So H" first="Hong-Seob" last="So">Hong-Seob So</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology, Wonkwang University, School of Medicine, Iksan, Jeonbuk, 54538, South Korea; Center for Metabolic Function Regulation, Wonkwang University, School of Medicine, Iksan, Jeonbuk, 54538, South Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Microbiology, Wonkwang University, School of Medicine, Iksan, Jeonbuk, 54538, South Korea; Center for Metabolic Function Regulation, Wonkwang University, School of Medicine, Iksan, Jeonbuk, 54538</wicri:regionArea><wicri:noRegion>54538</wicri:noRegion></affiliation></author><author><name sortKey="Park, Raekil" sort="Park, Raekil" uniqKey="Park R" first="Raekil" last="Park">Raekil Park</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biomedical Science & Engineering, GIST Research Institute, Gwangju Institute of Science & Technology, Gwangju, 61005, South Korea. Electronic address: rkpark@gist.ac.kr.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Biomedical Science & Engineering, GIST Research Institute, Gwangju Institute of Science & Technology, Gwangju, 61005</wicri:regionArea><wicri:noRegion>61005</wicri:noRegion></affiliation></author></analytic><series><title level="j">Biochemical and biophysical research communications</title><idno type="eISSN">1090-2104</idno><imprint><date when="2018" type="published">2018</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Autophagy (drug effects)</term><term>Cell Line (MeSH)</term><term>Cilia (drug effects)</term><term>Cilia (metabolism)</term><term>Humans (MeSH)</term><term>Retinal Pigment Epithelium (cytology)</term><term>Serum (metabolism)</term><term>Sirolimus (pharmacology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Autophagie (effets des médicaments et des substances chimiques)</term><term>Cils vibratiles (effets des médicaments et des substances chimiques)</term><term>Cils vibratiles (métabolisme)</term><term>Humains (MeSH)</term><term>Lignée cellulaire (MeSH)</term><term>Sirolimus (pharmacologie)</term><term>Sérum (métabolisme)</term><term>Épithélium pigmentaire de la rétine (cytologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Sirolimus</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Épithélium pigmentaire de la rétine</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Retinal Pigment Epithelium</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Autophagy</term><term>Cilia</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Autophagie</term><term>Cils vibratiles</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Cilia</term><term>Serum</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cils vibratiles</term><term>Sérum</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Sirolimus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line</term><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Humains</term><term>Lignée cellulaire</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Primary cilium is a microtubule structure that emanates from the surface of most human cells. Primary cilia assemble during the resting stage (G<sub>0</sub> phase) and disassemble with cell cycle progression. Defects associated with the control of the assembly or disassembly of the primary cilium have been implicated in various human diseases, including ciliopathy and cancer. Although studies have suggested the interplay between activation of autophagy and ciliogenesis, any direct mechanism between autophagy abatement and disassembly of primary cilium remains elusive. In this study, we found that the gradual abatement in autophagy during serum-restimulation was a dynamic process and significantly correlated with the disassembly of primary cilium in human retinal pigmented epithelial (RPE1) cells. Although autophagy activity was gradually decreased during serum-restimulation, the alteration in autophagy under the same condition prevented the disassembly of the primary cilium. Autophagy inhibitors such as chloroquine, U18666A and 3-methyladenine (3-MA) retained both the number of ciliated cells and cilium length. In contrast, rapamycin treatment during serum-restimulation maintained the number of ciliated cells with shortened cilia. Taken together, alteration in autophagy during serum-restimulation prevent the disassembly of the primary cilium, and autophagy modulators may serve as useful compounds for studying mechanistic details related to the disassembly of the primary cilium and ciliopathy.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">29649478</PMID><DateCompleted><Year>2018</Year><Month>09</Month><Day>19</Day></DateCompleted><DateRevised><Year>2018</Year><Month>09</Month><Day>19</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1090-2104</ISSN><JournalIssue CitedMedium="Internet"><Volume>500</Volume><Issue>2</Issue><PubDate><Year>2018</Year><Month>06</Month><Day>02</Day></PubDate></JournalIssue><Title>Biochemical and biophysical research communications</Title><ISOAbbreviation>Biochem Biophys Res Commun</ISOAbbreviation></Journal><ArticleTitle>Autophagy alteration prevents primary cilium disassembly in RPE1 cells.</ArticleTitle><Pagination><MedlinePgn>242-248</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0006-291X(18)30814-3</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.bbrc.2018.04.051</ELocationID><Abstract><AbstractText>Primary cilium is a microtubule structure that emanates from the surface of most human cells. Primary cilia assemble during the resting stage (G<sub>0</sub> phase) and disassemble with cell cycle progression. Defects associated with the control of the assembly or disassembly of the primary cilium have been implicated in various human diseases, including ciliopathy and cancer. Although studies have suggested the interplay between activation of autophagy and ciliogenesis, any direct mechanism between autophagy abatement and disassembly of primary cilium remains elusive. In this study, we found that the gradual abatement in autophagy during serum-restimulation was a dynamic process and significantly correlated with the disassembly of primary cilium in human retinal pigmented epithelial (RPE1) cells. Although autophagy activity was gradually decreased during serum-restimulation, the alteration in autophagy under the same condition prevented the disassembly of the primary cilium. Autophagy inhibitors such as chloroquine, U18666A and 3-methyladenine (3-MA) retained both the number of ciliated cells and cilium length. In contrast, rapamycin treatment during serum-restimulation maintained the number of ciliated cells with shortened cilia. Taken together, alteration in autophagy during serum-restimulation prevent the disassembly of the primary cilium, and autophagy modulators may serve as useful compounds for studying mechanistic details related to the disassembly of the primary cilium and ciliopathy.</AbstractText><CopyrightInformation>Copyright © 2018 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Maharjan</LastName><ForeName>Yunash</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Microbiology, Wonkwang University, School of Medicine, Iksan, Jeonbuk, 54538, South Korea; Center for Metabolic Function Regulation, Wonkwang University, School of Medicine, Iksan, Jeonbuk, 54538, South Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Joon No</ForeName><Initials>JN</Initials><AffiliationInfo><Affiliation>Department of Biomedical Science & Engineering, GIST Research Institute, Gwangju Institute of Science & Technology, Gwangju, 61005, South Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kwak</LastName><ForeName>SeongAe</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Zoonosis Research Center, Wonkwang University School of Medicine, Iksan, Jeonbuk, 54538, South Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lim</LastName><ForeName>Hyewon</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Microbiology, Wonkwang University, School of Medicine, Iksan, Jeonbuk, 54538, South Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dutta</LastName><ForeName>Raghbendra Kumar</ForeName><Initials>RK</Initials><AffiliationInfo><Affiliation>Department of Microbiology, Wonkwang University, School of Medicine, Iksan, Jeonbuk, 54538, South Korea; Center for Metabolic Function Regulation, Wonkwang University, School of Medicine, Iksan, Jeonbuk, 54538, South Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Zhi-Qiang</ForeName><Initials>ZQ</Initials><AffiliationInfo><Affiliation>Department of Microbiology, Wonkwang University, School of Medicine, Iksan, Jeonbuk, 54538, South Korea; Center for Metabolic Function Regulation, Wonkwang University, School of Medicine, Iksan, Jeonbuk, 54538, South Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>So</LastName><ForeName>Hong-Seob</ForeName><Initials>HS</Initials><AffiliationInfo><Affiliation>Department of Microbiology, Wonkwang University, School of Medicine, Iksan, Jeonbuk, 54538, South Korea; Center for Metabolic Function Regulation, Wonkwang University, School of Medicine, Iksan, Jeonbuk, 54538, South Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Park</LastName><ForeName>Raekil</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Biomedical Science & Engineering, GIST Research Institute, Gwangju Institute of Science & Technology, Gwangju, 61005, South Korea. Electronic address: rkpark@gist.ac.kr.</Affiliation></AffiliationInfo></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>2018</Year><Month>04</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Biochem Biophys Res Commun</MedlineTA><NlmUniqueID>0372516</NlmUniqueID><ISSNLinking>0006-291X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>W36ZG6FT64</RegistryNumber><NameOfSubstance UI="D020123">Sirolimus</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="Y">Autophagy</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002923" MajorTopicYN="N">Cilia</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D055213" MajorTopicYN="N">Retinal Pigment Epithelium</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="Y">cytology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D044967" MajorTopicYN="N">Serum</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020123" MajorTopicYN="N">Sirolimus</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Autophagy</Keyword><Keyword MajorTopicYN="Y">Cilia disassembly</Keyword><Keyword MajorTopicYN="Y">Ciliogenesis</Keyword><Keyword MajorTopicYN="Y">Primary cilia</Keyword><Keyword MajorTopicYN="Y">mTOR</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2018</Year><Month>03</Month><Day>31</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2018</Year><Month>04</Month><Day>07</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2018</Year><Month>4</Month><Day>13</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2018</Year><Month>9</Month><Day>20</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2018</Year><Month>4</Month><Day>13</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">29649478</ArticleId><ArticleId IdType="pii">S0006-291X(18)30814-3</ArticleId><ArticleId IdType="doi">10.1016/j.bbrc.2018.04.051</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Corée du Sud</li></country></list><tree><country name="Corée du Sud"><noRegion><name sortKey="Maharjan, Yunash" sort="Maharjan, Yunash" uniqKey="Maharjan Y" first="Yunash" last="Maharjan">Yunash Maharjan</name></noRegion><name sortKey="Dutta, Raghbendra Kumar" sort="Dutta, Raghbendra Kumar" uniqKey="Dutta R" first="Raghbendra Kumar" last="Dutta">Raghbendra Kumar Dutta</name><name sortKey="Kwak, Seongae" sort="Kwak, Seongae" uniqKey="Kwak S" first="Seongae" last="Kwak">Seongae Kwak</name><name sortKey="Lee, Joon No" sort="Lee, Joon No" uniqKey="Lee J" first="Joon No" last="Lee">Joon No Lee</name><name sortKey="Lim, Hyewon" sort="Lim, Hyewon" uniqKey="Lim H" first="Hyewon" last="Lim">Hyewon Lim</name><name sortKey="Liu, Zhi Qiang" sort="Liu, Zhi Qiang" uniqKey="Liu Z" first="Zhi-Qiang" last="Liu">Zhi-Qiang Liu</name><name sortKey="Park, Raekil" sort="Park, Raekil" uniqKey="Park R" first="Raekil" last="Park">Raekil Park</name><name sortKey="So, Hong Seob" sort="So, Hong Seob" uniqKey="So H" first="Hong-Seob" last="So">Hong-Seob So</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Bois/explor/RapamycinFungusV1/Data/Main/Exploration
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{{Explor lien
|wiki= Bois
|area= RapamycinFungusV1
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|clé= pubmed:29649478
|texte= Autophagy alteration prevents primary cilium disassembly in RPE1 cells.
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