DetoxFungiV1, Main, Exploration, bibRecord, 000436

Mitochondrial lipid droplet formation as a detoxification mechanism to sequester and degrade excessive urothelial membranes.

Identifieur interne : 000436 ( Main/Exploration ); précédent : 000435; suivant : 000437

Mitochondrial lipid droplet formation as a detoxification mechanism to sequester and degrade excessive urothelial membranes.

Auteurs : Yi Liao ; Daniel K L. Tham ; Feng-Xia Liang ; Jennifer Chang ; Yuan Wei ; Putty-Reddy Sudhir ; Joseph Sall ; Sarah J. Ren ; Javier U. Chicote [Espagne] ; Lora L. Arnold [États-Unis] ; Chih-Chi Andrew Hu [États-Unis] ; Rok Romih [Slovénie] ; Leonardo R. Andrade [États-Unis] ; Michael J. Rindler ; Samuel M. Cohen [États-Unis] ; Rob Desalle [États-Unis] ; Antonio Garcia-Espa A [Espagne] ; Mingxiao Ding [République populaire de Chine] ; Xue-Ru Wu [États-Unis] ; Tung-Tien Sun

Source :

Molecular biology of the cell [ 1939-4586 ] ; 2019.

RBID : pubmed:31577526

Descripteurs français

KwdFr :
- Animaux (MeSH), Corps multivésiculaires (métabolisme), Femelle (MeSH), Glycoprotéines membranaires (métabolisme), Gouttelettes lipidiques (métabolisme), Gouttelettes lipidiques (physiologie), Membranes (métabolisme), Mitochondries (métabolisme), Nexines de tri (métabolisme), Souris (MeSH), Souris de lignée C57BL (MeSH), Uroplakines (métabolisme), Uroplakines (physiologie), Urothélium (métabolisme), Vessie urinaire (métabolisme).
MESH :
- métabolisme : Corps multivésiculaires, Glycoprotéines membranaires, Gouttelettes lipidiques, Membranes, Mitochondries, Nexines de tri, Uroplakines, Urothélium, Vessie urinaire.
- physiologie : Gouttelettes lipidiques, Uroplakines.
- Animaux, Femelle, Souris, Souris de lignée C57BL.

English descriptors

KwdEn :
- Animals (MeSH), Female (MeSH), Lipid Droplets (metabolism), Lipid Droplets (physiology), Membrane Glycoproteins (metabolism), Membranes (metabolism), Mice (MeSH), Mice, Inbred C57BL (MeSH), Mitochondria (metabolism), Multivesicular Bodies (metabolism), Sorting Nexins (metabolism), Urinary Bladder (metabolism), Uroplakins (metabolism), Uroplakins (physiology), Urothelium (metabolism).
MESH :
- chemical , metabolism : Membrane Glycoproteins, Sorting Nexins, Uroplakins.
- metabolism : Lipid Droplets, Membranes, Mitochondria, Multivesicular Bodies, Urinary Bladder, Urothelium.
- physiology : Lipid Droplets, Uroplakins.
- Animals, Female, Mice, Mice, Inbred C57BL.

Abstract

The apical surface of the terminally differentiated mammalian urothelial umbrella cell is mechanically stable and highly impermeable, in part due to its coverage by urothelial plaques consisting of 2D crystals of uroplakin particles. The mechanism for regulating the uroplakin/plaque level is unclear. We found that genetic ablation of the highly tissue-specific sorting nexin Snx31, which localizes to plaques lining the multivesicular bodies (MVBs) in urothelial umbrella cells, abolishes MVBs suggesting that Snx31 plays a role in stabilizing the MVB-associated plaques by allowing them to achieve a greater curvature. Strikingly, Snx31 ablation also induces a massive accumulation of uroplakin-containing mitochondria-derived lipid droplets (LDs), which mediate uroplakin degradation via autophagy/lipophagy, leading to the loss of apical and fusiform vesicle plaques. These results suggest that MVBs play an active role in suppressing the excessive/wasteful endocytic degradation of uroplakins. Failure of this suppression mechanism triggers the formation of mitochondrial LDs so that excessive uroplakin membranes can be sequestered and degraded. Because mitochondrial LD formation, which occurs at a low level in normal urothelium, can also be induced by disturbance in uroplakin polymerization due to individual uroplakin knockout and by arsenite, a bladder carcinogen, this pathway may represent an inducible, versatile urothelial detoxification mechanism.

DOI: 10.1091/mbc.E19-05-0284
PubMed: 31577526
PubMed Central: PMC6857570

Affiliations:

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

to stream Main, to step Corpus: 000324
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Le document en format XML

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<author><name sortKey="Sun, Tung Tien" sort="Sun, Tung Tien" uniqKey="Sun T" first="Tung-Tien" last="Sun">Tung-Tien Sun</name>
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<affiliation><nlm:affiliation>Department of Urology, New York University School of Medicine, New York, NY10016.</nlm:affiliation>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Mitochondrial lipid droplet formation as a detoxification mechanism to sequester and degrade excessive urothelial membranes.</title>
<author><name sortKey="Liao, Yi" sort="Liao, Yi" uniqKey="Liao Y" first="Yi" last="Liao">Yi Liao</name>
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<wicri:noCountry code="subField">NY10016</wicri:noCountry>
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<author><name sortKey="Tham, Daniel K L" sort="Tham, Daniel K L" uniqKey="Tham D" first="Daniel K L" last="Tham">Daniel K L. Tham</name>
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<wicri:noCountry code="subField">NY10016</wicri:noCountry>
</affiliation>
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<author><name sortKey="Liang, Feng Xia" sort="Liang, Feng Xia" uniqKey="Liang F" first="Feng-Xia" last="Liang">Feng-Xia Liang</name>
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<wicri:noCountry code="subField">NY10016</wicri:noCountry>
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<author><name sortKey="Chang, Jennifer" sort="Chang, Jennifer" uniqKey="Chang J" first="Jennifer" last="Chang">Jennifer Chang</name>
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<wicri:noCountry code="subField">NY10016</wicri:noCountry>
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<author><name sortKey="Wei, Yuan" sort="Wei, Yuan" uniqKey="Wei Y" first="Yuan" last="Wei">Yuan Wei</name>
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<wicri:noCountry code="subField">NY10016</wicri:noCountry>
</affiliation>
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<wicri:noCountry code="subField">NY10016</wicri:noCountry>
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<wicri:noCountry code="subField">NY10016</wicri:noCountry>
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<country xml:lang="fr">Espagne</country>
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<author><name sortKey="Andrade, Leonardo R" sort="Andrade, Leonardo R" uniqKey="Andrade L" first="Leonardo R" last="Andrade">Leonardo R. Andrade</name>
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</placeName>
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<author><name sortKey="Cohen, Samuel M" sort="Cohen, Samuel M" uniqKey="Cohen S" first="Samuel M" last="Cohen">Samuel M. Cohen</name>
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<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Nebraska</region>
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<author><name sortKey="Desalle, Rob" sort="Desalle, Rob" uniqKey="Desalle R" first="Rob" last="Desalle">Rob Desalle</name>
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<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">État de New York</region>
</placeName>
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</affiliation>
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<author><name sortKey="Garcia Espa A, Antonio" sort="Garcia Espa A, Antonio" uniqKey="Garcia Espa A A" first="Antonio" last="Garcia-Espa A">Antonio Garcia-Espa A</name>
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<country xml:lang="fr">Espagne</country>
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<placeName><region nuts="2" type="communauté">Catalogne</region>
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<author><name sortKey="Ding, Mingxiao" sort="Ding, Mingxiao" uniqKey="Ding M" first="Mingxiao" last="Ding">Mingxiao Ding</name>
<affiliation wicri:level="4"><nlm:affiliation>College of Life Sciences, Peking University, Dachengfang, Haidian, Beijing 100871, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>College of Life Sciences, Peking University, Dachengfang, Haidian, Beijing 100871</wicri:regionArea>
<placeName><settlement type="city">Pékin</settlement>
</placeName>
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<placeName><settlement type="city">Pékin</settlement>
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</placeName>
</affiliation>
</author>
<author><name sortKey="Wu, Xue Ru" sort="Wu, Xue Ru" uniqKey="Wu X" first="Xue-Ru" last="Wu">Xue-Ru Wu</name>
<affiliation><nlm:affiliation>Department of Urology, New York University School of Medicine, New York, NY10016.</nlm:affiliation>
<wicri:noCountry code="subField">NY10016</wicri:noCountry>
</affiliation>
<affiliation><nlm:affiliation>Department of Pathology, New York University School of Medicine, New York, NY10016.</nlm:affiliation>
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<author><name sortKey="Sun, Tung Tien" sort="Sun, Tung Tien" uniqKey="Sun T" first="Tung-Tien" last="Sun">Tung-Tien Sun</name>
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<affiliation><nlm:affiliation>Department of Urology, New York University School of Medicine, New York, NY10016.</nlm:affiliation>
<wicri:noCountry code="subField">NY10016</wicri:noCountry>
</affiliation>
<affiliation><nlm:affiliation>Department of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, NY10016.</nlm:affiliation>
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</affiliation>
<affiliation><nlm:affiliation>Department of Dermatology, New York University School of Medicine, New York, NY10016.</nlm:affiliation>
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<series><title level="j">Molecular biology of the cell</title>
<idno type="eISSN">1939-4586</idno>
<imprint><date when="2019" type="published">2019</date>
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<term>Female (MeSH)</term>
<term>Lipid Droplets (metabolism)</term>
<term>Lipid Droplets (physiology)</term>
<term>Membrane Glycoproteins (metabolism)</term>
<term>Membranes (metabolism)</term>
<term>Mice (MeSH)</term>
<term>Mice, Inbred C57BL (MeSH)</term>
<term>Mitochondria (metabolism)</term>
<term>Multivesicular Bodies (metabolism)</term>
<term>Sorting Nexins (metabolism)</term>
<term>Urinary Bladder (metabolism)</term>
<term>Uroplakins (metabolism)</term>
<term>Uroplakins (physiology)</term>
<term>Urothelium (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term>
<term>Corps multivésiculaires (métabolisme)</term>
<term>Femelle (MeSH)</term>
<term>Glycoprotéines membranaires (métabolisme)</term>
<term>Gouttelettes lipidiques (métabolisme)</term>
<term>Gouttelettes lipidiques (physiologie)</term>
<term>Membranes (métabolisme)</term>
<term>Mitochondries (métabolisme)</term>
<term>Nexines de tri (métabolisme)</term>
<term>Souris (MeSH)</term>
<term>Souris de lignée C57BL (MeSH)</term>
<term>Uroplakines (métabolisme)</term>
<term>Uroplakines (physiologie)</term>
<term>Urothélium (métabolisme)</term>
<term>Vessie urinaire (métabolisme)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Membrane Glycoproteins</term>
<term>Sorting Nexins</term>
<term>Uroplakins</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Lipid Droplets</term>
<term>Membranes</term>
<term>Mitochondria</term>
<term>Multivesicular Bodies</term>
<term>Urinary Bladder</term>
<term>Urothelium</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Corps multivésiculaires</term>
<term>Glycoprotéines membranaires</term>
<term>Gouttelettes lipidiques</term>
<term>Membranes</term>
<term>Mitochondries</term>
<term>Nexines de tri</term>
<term>Uroplakines</term>
<term>Urothélium</term>
<term>Vessie urinaire</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Gouttelettes lipidiques</term>
<term>Uroplakines</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Lipid Droplets</term>
<term>Uroplakins</term>
</keywords>
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<term>Female</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Femelle</term>
<term>Souris</term>
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<front><div type="abstract" xml:lang="en">The apical surface of the terminally differentiated mammalian urothelial umbrella cell is mechanically stable and highly impermeable, in part due to its coverage by urothelial plaques consisting of 2D crystals of uroplakin particles. The mechanism for regulating the uroplakin/plaque level is unclear. We found that genetic ablation of the highly tissue-specific sorting nexin Snx31, which localizes to plaques lining the multivesicular bodies (MVBs) in urothelial umbrella cells, abolishes MVBs suggesting that Snx31 plays a role in stabilizing the MVB-associated plaques by allowing them to achieve a greater curvature. Strikingly, Snx31 ablation also induces a massive accumulation of uroplakin-containing mitochondria-derived lipid droplets (LDs), which mediate uroplakin degradation via autophagy/lipophagy, leading to the loss of apical and fusiform vesicle plaques. These results suggest that MVBs play an active role in suppressing the excessive/wasteful endocytic degradation of uroplakins. Failure of this suppression mechanism triggers the formation of mitochondrial LDs so that excessive uroplakin membranes can be sequestered and degraded. Because mitochondrial LD formation, which occurs at a low level in normal urothelium, can also be induced by disturbance in uroplakin polymerization due to individual uroplakin knockout and by arsenite, a bladder carcinogen, this pathway may represent an inducible, versatile urothelial detoxification mechanism.</div>
</front>
</TEI>
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<DateCompleted><Year>2020</Year>
<Month>05</Month>
<Day>18</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>06</Month>
<Day>13</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1939-4586</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>30</Volume>
<Issue>24</Issue>
<PubDate><Year>2019</Year>
<Month>11</Month>
<Day>15</Day>
</PubDate>
</JournalIssue>
<Title>Molecular biology of the cell</Title>
<ISOAbbreviation>Mol Biol Cell</ISOAbbreviation>
</Journal>
<ArticleTitle>Mitochondrial lipid droplet formation as a detoxification mechanism to sequester and degrade excessive urothelial membranes.</ArticleTitle>
<Pagination><MedlinePgn>2969-2984</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1091/mbc.E19-05-0284</ELocationID>
<Abstract><AbstractText>The apical surface of the terminally differentiated mammalian urothelial umbrella cell is mechanically stable and highly impermeable, in part due to its coverage by urothelial plaques consisting of 2D crystals of uroplakin particles. The mechanism for regulating the uroplakin/plaque level is unclear. We found that genetic ablation of the highly tissue-specific sorting nexin Snx31, which localizes to plaques lining the multivesicular bodies (MVBs) in urothelial umbrella cells, abolishes MVBs suggesting that Snx31 plays a role in stabilizing the MVB-associated plaques by allowing them to achieve a greater curvature. Strikingly, Snx31 ablation also induces a massive accumulation of uroplakin-containing mitochondria-derived lipid droplets (LDs), which mediate uroplakin degradation via autophagy/lipophagy, leading to the loss of apical and fusiform vesicle plaques. These results suggest that MVBs play an active role in suppressing the excessive/wasteful endocytic degradation of uroplakins. Failure of this suppression mechanism triggers the formation of mitochondrial LDs so that excessive uroplakin membranes can be sequestered and degraded. Because mitochondrial LD formation, which occurs at a low level in normal urothelium, can also be induced by disturbance in uroplakin polymerization due to individual uroplakin knockout and by arsenite, a bladder carcinogen, this pathway may represent an inducible, versatile urothelial detoxification mechanism.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Liao</LastName>
<ForeName>Yi</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Department of Cell Biology, New York University School of Medicine, New York, NY10016.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Tham</LastName>
<ForeName>Daniel K L</ForeName>
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<AffiliationInfo><Affiliation>Department of Cell Biology, New York University School of Medicine, New York, NY10016.</Affiliation>
</AffiliationInfo>
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<ForeName>Feng-Xia</ForeName>
<Initials>FX</Initials>
<AffiliationInfo><Affiliation>Department of Cell Biology, New York University School of Medicine, New York, NY10016.</Affiliation>
</AffiliationInfo>
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<ForeName>Jennifer</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Cell Biology, New York University School of Medicine, New York, NY10016.</Affiliation>
</AffiliationInfo>
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<ForeName>Yuan</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Department of Cell Biology, New York University School of Medicine, New York, NY10016.</Affiliation>
</AffiliationInfo>
</Author>
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<ForeName>Putty-Reddy</ForeName>
<Initials>PR</Initials>
<AffiliationInfo><Affiliation>Department of Cell Biology, New York University School of Medicine, New York, NY10016.</Affiliation>
</AffiliationInfo>
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<ForeName>Joseph</ForeName>
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</AffiliationInfo>
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<ForeName>Sarah J</ForeName>
<Initials>SJ</Initials>
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</AffiliationInfo>
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<ForeName>Javier U</ForeName>
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<AffiliationInfo><Affiliation>Research Unit, Hospital Joan XXIII, Institut de Investigacio Sanitaria Pere Virgili (IISPV), Universitat Rovira i Virgili, Tarragona 43007, Spain.</Affiliation>
</AffiliationInfo>
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<ForeName>Lora L</ForeName>
<Initials>LL</Initials>
<AffiliationInfo><Affiliation>Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198.</Affiliation>
</AffiliationInfo>
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<ForeName>Chih-Chi Andrew</ForeName>
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<AffiliationInfo><Affiliation>The Wistar Institute, University of Pennsylvania, Philadelphia, PA 19104.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Romih</LastName>
<ForeName>Rok</ForeName>
<Initials>R</Initials>
<AffiliationInfo><Affiliation>Institute of Cell Biology, Faculty of Medicine, University of Ljubljana, SI-1000 Ljubljana, Slovenia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Andrade</LastName>
<ForeName>Leonardo R</ForeName>
<Initials>LR</Initials>
<AffiliationInfo><Affiliation>Salk Institute, La Jolla, CA 92037.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Rindler</LastName>
<ForeName>Michael J</ForeName>
<Initials>MJ</Initials>
<AffiliationInfo><Affiliation>Department of Cell Biology, New York University School of Medicine, New York, NY10016.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Cohen</LastName>
<ForeName>Samuel M</ForeName>
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<AffiliationInfo><Affiliation>Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>DeSalle</LastName>
<ForeName>Rob</ForeName>
<Initials>R</Initials>
<AffiliationInfo><Affiliation>Sackler Institute for Comparative Genomics, American Museum of Natural History, New York, NY 10024.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Garcia-España</LastName>
<ForeName>Antonio</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Research Unit, Hospital Joan XXIII, Institut de Investigacio Sanitaria Pere Virgili (IISPV), Universitat Rovira i Virgili, Tarragona 43007, Spain.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Ding</LastName>
<ForeName>Mingxiao</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>College of Life Sciences, Peking University, Dachengfang, Haidian, Beijing 100871, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wu</LastName>
<ForeName>Xue-Ru</ForeName>
<Initials>XR</Initials>
<AffiliationInfo><Affiliation>Department of Urology, New York University School of Medicine, New York, NY10016.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Pathology, New York University School of Medicine, New York, NY10016.</Affiliation>
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<AffiliationInfo><Affiliation>Veterans Affairs Medical Center, New York, NY 10010.</Affiliation>
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<ForeName>Tung-Tien</ForeName>
<Initials>TT</Initials>
<AffiliationInfo><Affiliation>Department of Cell Biology, New York University School of Medicine, New York, NY10016.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Urology, New York University School of Medicine, New York, NY10016.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, NY10016.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Dermatology, New York University School of Medicine, New York, NY10016.</Affiliation>
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	Serveur d'exploration sur la détoxication des champignons
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Mitochondrial lipid droplet formation as a detoxification mechanism to sequester and degrade excessive urothelial membranes.

Mitochondrial lipid droplet formation as a detoxification mechanism to sequester and degrade excessive urothelial membranes.

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