LymphedemaV1, Main, Exploration, bibRecord, 001D96

FOXC2 and fluid shear stress stabilize postnatal lymphatic vasculature

Identifieur interne : 001D96 ( Main/Exploration ); précédent : 001D95; suivant : 001D97

FOXC2 and fluid shear stress stabilize postnatal lymphatic vasculature

Auteurs : Amélie Sabine [Suisse] ; Esther Bovay [Suisse] ; Cansaran Saygili Demir [Suisse] ; Wataru Kimura [Japon] ; Muriel Jaquet [Suisse] ; Yan Agalarov [Suisse] ; Nadine Zangger [Suisse] ; Joshua P. Scallan [États-Unis] ; Werner Graber [Suisse] ; Elgin Gulpinar [États-Unis] ; Brenda R. Kwak [Suisse] ; Taija M Kinen [Suède] ; Inés Martinez-Corral [Espagne] ; Sagrario Ortega [Espagne] ; Mauro Delorenzi [Suisse] ; Friedemann Kiefer [Allemagne] ; Michael J. Davis [États-Unis] ; Valentin Djonov [Suisse] ; Naoyuki Miura [Japon] ; Tatiana V. Petrova [Suisse]

Source :

The Journal of Clinical Investigation [ 0021-9738 ] ; 2015.

RBID : PMC:4607114

Descripteurs français

KwdFr :
- Animaux, Apoptose, Cellules cultivées, Cellules endothéliales (anatomopathologie), Cellules endothéliales (cytologie), Contrainte mécanique, Cycle cellulaire, Cytosquelette (ultrastructure), Division cellulaire, Facteurs de transcription (physiologie), Facteurs de transcription Forkhead (antagonistes et inhibiteurs), Facteurs de transcription Forkhead (déficit), Facteurs de transcription Forkhead (physiologie), Fibres de stress (ultrastructure), Humains, Interférence par ARN, Jonctions intercellulaires (ultrastructure), Petit ARN interférent (pharmacologie), Phosphoprotéines (physiologie), Protéines adaptatrices de la transduction du signal (physiologie), Rhéologie, Souris, Souris de lignée C57BL, Souris knockout, Système lymphatique (croissance et développement), Transcription génétique, Transfection, Vaisseaux lymphatiques (anatomopathologie), Vaisseaux lymphatiques (cytologie).
MESH :
- anatomopathologie : Cellules endothéliales, Vaisseaux lymphatiques.
- antagonistes et inhibiteurs : Facteurs de transcription Forkhead.
- croissance et développement : Système lymphatique.
- cytologie : Cellules endothéliales, Vaisseaux lymphatiques.
- déficit : Facteurs de transcription Forkhead.
- pharmacologie : Petit ARN interférent.
- physiologie : Facteurs de transcription, Facteurs de transcription Forkhead, Phosphoprotéines, Protéines adaptatrices de la transduction du signal.
- ultrastructure : Animaux, Apoptose, Cellules cultivées, Contrainte mécanique, Cycle cellulaire, Cytosquelette, Division cellulaire, Fibres de stress, Humains, Interférence par ARN, Jonctions intercellulaires, Rhéologie, Souris, Souris de lignée C57BL, Souris knockout, Transcription génétique, Transfection.

English descriptors

KwdEn :
- Adaptor Proteins, Signal Transducing (physiology), Animals, Apoptosis, Cell Cycle, Cell Division, Cells, Cultured, Cytoskeleton (ultrastructure), Endothelial Cells (cytology), Endothelial Cells (pathology), Forkhead Transcription Factors (antagonists & inhibitors), Forkhead Transcription Factors (deficiency), Forkhead Transcription Factors (physiology), Humans, Intercellular Junctions (ultrastructure), Lymphatic System (growth & development), Lymphatic Vessels (cytology), Lymphatic Vessels (pathology), Mice, Mice, Inbred C57BL, Mice, Knockout, Phosphoproteins (physiology), RNA Interference, RNA, Small Interfering (pharmacology), Rheology, Stress Fibers (ultrastructure), Stress, Mechanical, Transcription Factors (physiology), Transcription, Genetic, Transfection.
MESH :
- chemical , antagonists & inhibitors : Forkhead Transcription Factors.
- chemical , deficiency : Forkhead Transcription Factors.
- chemical , pharmacology : RNA, Small Interfering.
- chemical , physiology : Adaptor Proteins, Signal Transducing, Forkhead Transcription Factors, Phosphoproteins, Transcription Factors.
- cytology : Endothelial Cells, Lymphatic Vessels.
- growth & development : Lymphatic System.
- pathology : Endothelial Cells, Lymphatic Vessels.
- ultrastructure : Cytoskeleton, Intercellular Junctions, Stress Fibers.
- Animals, Apoptosis, Cell Cycle, Cell Division, Cells, Cultured, Humans, Mice, Mice, Inbred C57BL, Mice, Knockout, RNA Interference, Rheology, Stress, Mechanical, Transcription, Genetic, Transfection.

Abstract

Biomechanical forces, such as fluid shear stress, govern multiple aspects of endothelial cell biology. In blood vessels, disturbed flow is associated with vascular diseases, such as atherosclerosis, and promotes endothelial cell proliferation and apoptosis. Here, we identified an important role for disturbed flow in lymphatic vessels, in which it cooperates with the transcription factor FOXC2 to ensure lifelong stability of the lymphatic vasculature. In cultured lymphatic endothelial cells, FOXC2 inactivation conferred abnormal shear stress sensing, promoting junction disassembly and entry into the cell cycle. Loss of FOXC2-dependent quiescence was mediated by the Hippo pathway transcriptional coactivator TAZ and, ultimately, led to cell death. In murine models, inducible deletion of Foxc2 within the lymphatic vasculature led to cell-cell junction defects, regression of valves, and focal vascular lumen collapse, which triggered generalized lymphatic vascular dysfunction and lethality. Together, our work describes a fundamental mechanism by which FOXC2 and oscillatory shear stress maintain lymphatic endothelial cell quiescence through intercellular junction and cytoskeleton stabilization and provides an essential link between biomechanical forces and endothelial cell identity that is necessary for postnatal vessel homeostasis. As FOXC2 is mutated in lymphedema-distichiasis syndrome, our data also underscore the role of impaired mechanotransduction in the pathology of this hereditary human disease.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4607114

DOI: 10.1172/JCI80454
PubMed: 26389677
PubMed Central: 4607114

Affiliations:

Le document en format XML

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<author><name sortKey="Jaquet, Muriel" sort="Jaquet, Muriel" uniqKey="Jaquet M" first="Muriel" last="Jaquet">Muriel Jaquet</name>
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<author><name sortKey="Martinez Corral, Ines" sort="Martinez Corral, Ines" uniqKey="Martinez Corral I" first="Inés" last="Martinez-Corral">Inés Martinez-Corral</name>
<affiliation wicri:level="3"><nlm:aff id="A9">Spanish National Cancer Research Centre, Madrid, Spain.</nlm:aff>
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<wicri:regionArea>Spanish National Cancer Research Centre, Madrid</wicri:regionArea>
<placeName><settlement type="city">Madrid</settlement>
<region nuts="2" type="region">Communauté de Madrid</region>
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<author><name sortKey="Ortega, Sagrario" sort="Ortega, Sagrario" uniqKey="Ortega S" first="Sagrario" last="Ortega">Sagrario Ortega</name>
<affiliation wicri:level="3"><nlm:aff id="A9">Spanish National Cancer Research Centre, Madrid, Spain.</nlm:aff>
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<author><name sortKey="Delorenzi, Mauro" sort="Delorenzi, Mauro" uniqKey="Delorenzi M" first="Mauro" last="Delorenzi">Mauro Delorenzi</name>
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<wicri:regionArea>Ludwig Center for Cancer Research, University Lausanne, Lausanne</wicri:regionArea>
<placeName><settlement type="city">Lausanne</settlement>
<region nuts="3" type="region">Canton de Vaud</region>
</placeName>
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<author><name sortKey="Kiefer, Friedemann" sort="Kiefer, Friedemann" uniqKey="Kiefer F" first="Friedemann" last="Kiefer">Friedemann Kiefer</name>
<affiliation wicri:level="3"><nlm:aff id="A11">Max Planck Institute for Molecular Biomedicine, Münster, Germany.</nlm:aff>
<country xml:lang="fr" wicri:curation="lc">Allemagne</country>
<wicri:regionArea>Max Planck Institute for Molecular Biomedicine, Münster</wicri:regionArea>
<placeName><region type="land" nuts="1">Rhénanie-du-Nord-Westphalie</region>
<region type="district" nuts="2">District de Münster</region>
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</placeName>
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<author><name sortKey="Davis, Michael J" sort="Davis, Michael J" uniqKey="Davis M" first="Michael J." last="Davis">Michael J. Davis</name>
<affiliation wicri:level="2"><nlm:aff id="A4">University of Missouri, Columbia, Missouri, USA.</nlm:aff>
<country xml:lang="fr" wicri:curation="lc">États-Unis</country>
<wicri:regionArea>University of Missouri, Columbia, Missouri</wicri:regionArea>
<placeName><region type="state">Missouri (État)</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Djonov, Valentin" sort="Djonov, Valentin" uniqKey="Djonov V" first="Valentin" last="Djonov">Valentin Djonov</name>
<affiliation wicri:level="4"><nlm:aff id="A5">Institute of Anatomy, University of Bern, Bern, Switzerland.</nlm:aff>
<country xml:lang="fr" wicri:curation="lc">Suisse</country>
<wicri:regionArea>Institute of Anatomy, University of Bern, Bern</wicri:regionArea>
<placeName><settlement type="city">Berne</settlement>
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<settlement type="city">Berne</settlement>
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<author><name sortKey="Miura, Naoyuki" sort="Miura, Naoyuki" uniqKey="Miura N" first="Naoyuki" last="Miura">Naoyuki Miura</name>
<affiliation wicri:level="1"><nlm:aff id="A2">Hamamatsu University School of Medicine, Hamamatsu, Japan.</nlm:aff>
<country xml:lang="fr" wicri:curation="lc">Japon</country>
<wicri:regionArea>Hamamatsu University School of Medicine, Hamamatsu</wicri:regionArea>
<wicri:noRegion>Hamamatsu</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Petrova, Tatiana V" sort="Petrova, Tatiana V" uniqKey="Petrova T" first="Tatiana V." last="Petrova">Tatiana V. Petrova</name>
<affiliation wicri:level="1"><nlm:aff id="A1">Department of Fundamental Oncology, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Epalinges, Switzerland.</nlm:aff>
<country xml:lang="fr" wicri:curation="lc">Suisse</country>
<wicri:regionArea>Department of Fundamental Oncology, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Epalinges</wicri:regionArea>
<wicri:noRegion>Epalinges</wicri:noRegion>
</affiliation>
<affiliation wicri:level="3"><nlm:aff id="A12">Swiss Cancer Research Institute, École Polytechnique Fédérale de Lausanne, Lausanne, Switzerland.</nlm:aff>
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<wicri:regionArea>Swiss Cancer Research Institute, École Polytechnique Fédérale de Lausanne, Lausanne</wicri:regionArea>
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<series><title level="j">The Journal of Clinical Investigation</title>
<idno type="ISSN">0021-9738</idno>
<idno type="eISSN">1558-8238</idno>
<imprint><date when="2015">2015</date>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adaptor Proteins, Signal Transducing (physiology)</term>
<term>Animals</term>
<term>Apoptosis</term>
<term>Cell Cycle</term>
<term>Cell Division</term>
<term>Cells, Cultured</term>
<term>Cytoskeleton (ultrastructure)</term>
<term>Endothelial Cells (cytology)</term>
<term>Endothelial Cells (pathology)</term>
<term>Forkhead Transcription Factors (antagonists & inhibitors)</term>
<term>Forkhead Transcription Factors (deficiency)</term>
<term>Forkhead Transcription Factors (physiology)</term>
<term>Humans</term>
<term>Intercellular Junctions (ultrastructure)</term>
<term>Lymphatic System (growth & development)</term>
<term>Lymphatic Vessels (cytology)</term>
<term>Lymphatic Vessels (pathology)</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Knockout</term>
<term>Phosphoproteins (physiology)</term>
<term>RNA Interference</term>
<term>RNA, Small Interfering (pharmacology)</term>
<term>Rheology</term>
<term>Stress Fibers (ultrastructure)</term>
<term>Stress, Mechanical</term>
<term>Transcription Factors (physiology)</term>
<term>Transcription, Genetic</term>
<term>Transfection</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term>
<term>Apoptose</term>
<term>Cellules cultivées</term>
<term>Cellules endothéliales (anatomopathologie)</term>
<term>Cellules endothéliales (cytologie)</term>
<term>Contrainte mécanique</term>
<term>Cycle cellulaire</term>
<term>Cytosquelette (ultrastructure)</term>
<term>Division cellulaire</term>
<term>Facteurs de transcription (physiologie)</term>
<term>Facteurs de transcription Forkhead (antagonistes et inhibiteurs)</term>
<term>Facteurs de transcription Forkhead (déficit)</term>
<term>Facteurs de transcription Forkhead (physiologie)</term>
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<term>Humains</term>
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<term>Jonctions intercellulaires (ultrastructure)</term>
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<term>Système lymphatique (croissance et développement)</term>
<term>Transcription génétique</term>
<term>Transfection</term>
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<term>Vaisseaux lymphatiques (cytologie)</term>
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<term>Phosphoproteins</term>
<term>Transcription Factors</term>
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<term>Vaisseaux lymphatiques</term>
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<keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Facteurs de transcription Forkhead</term>
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<keywords scheme="MESH" qualifier="croissance et développement" xml:lang="fr"><term>Système lymphatique</term>
</keywords>
<keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Cellules endothéliales</term>
<term>Vaisseaux lymphatiques</term>
</keywords>
<keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Endothelial Cells</term>
<term>Lymphatic Vessels</term>
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<keywords scheme="MESH" qualifier="déficit" xml:lang="fr"><term>Facteurs de transcription Forkhead</term>
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<keywords scheme="MESH" qualifier="ultrastructure" xml:lang="fr"><term>Animaux</term>
<term>Apoptose</term>
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<term>Rhéologie</term>
<term>Souris</term>
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<term>Souris knockout</term>
<term>Transcription génétique</term>
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<front><div type="abstract" xml:lang="en"><p>Biomechanical forces, such as fluid shear stress, govern multiple aspects of endothelial cell biology. In blood vessels, disturbed flow is associated with vascular diseases, such as atherosclerosis, and promotes endothelial cell proliferation and apoptosis. Here, we identified an important role for disturbed flow in lymphatic vessels, in which it cooperates with the transcription factor FOXC2 to ensure lifelong stability of the lymphatic vasculature. In cultured lymphatic endothelial cells, <italic>FOXC2</italic>
 inactivation conferred abnormal shear stress sensing, promoting junction disassembly and entry into the cell cycle. Loss of FOXC2-dependent quiescence was mediated by the Hippo pathway transcriptional coactivator TAZ and, ultimately, led to cell death. In murine models, inducible deletion of <italic>Foxc2</italic>
 within the lymphatic vasculature led to cell-cell junction defects, regression of valves, and focal vascular lumen collapse, which triggered generalized lymphatic vascular dysfunction and lethality. Together, our work describes a fundamental mechanism by which FOXC2 and oscillatory shear stress maintain lymphatic endothelial cell quiescence through intercellular junction and cytoskeleton stabilization and provides an essential link between biomechanical forces and endothelial cell identity that is necessary for postnatal vessel homeostasis. As <italic>FOXC2</italic>
 is mutated in lymphedema-distichiasis syndrome, our data also underscore the role of impaired mechanotransduction in the pathology of this hereditary human disease.</p>
</div>
</front>
</TEI>
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<name sortKey="Zangger, Nadine" sort="Zangger, Nadine" uniqKey="Zangger N" first="Nadine" last="Zangger">Nadine Zangger</name>
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<country name="Japon"><noRegion><name sortKey="Kimura, Wataru" sort="Kimura, Wataru" uniqKey="Kimura W" first="Wataru" last="Kimura">Wataru Kimura</name>
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<name sortKey="Miura, Naoyuki" sort="Miura, Naoyuki" uniqKey="Miura N" first="Naoyuki" last="Miura">Naoyuki Miura</name>
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<country name="Espagne"><region name="Communauté de Madrid"><name sortKey="Martinez Corral, Ines" sort="Martinez Corral, Ines" uniqKey="Martinez Corral I" first="Inés" last="Martinez-Corral">Inés Martinez-Corral</name>
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FOXC2 and fluid shear stress stabilize postnatal lymphatic vasculature

FOXC2 and fluid shear stress stabilize postnatal lymphatic vasculature

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