Vimentin intermediate filament assembly regulates fibroblast invasion in fibrogenic lung injury
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Auteurs : Ranu Surolia ; Fu Jun Li ; Zheng Wang ; Huashi Li ; Kevin Dsouza ; Vinoy Thomas ; Sergey Mirov [États-Unis] ; Dolores Pérez-Sala [Espagne] ; Mohammad Athar [États-Unis] ; Victor J. Thannickal ; Veena B. AntonySource :
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Abstract
Idiopathic pulmonary fibrosis (IPF) is a progressive disease, with a median survival of 3–5 years following diagnosis. Lung remodeling by invasive fibroblasts is a hallmark of IPF. In this study, we demonstrate that inhibition of vimentin intermediate filaments (VimIFs) decreases the invasiveness of IPF fibroblasts and confers protection against fibrosis in a murine model of experimental lung injury. Increased expression and organization of VimIFs contribute to the invasive property of IPF fibroblasts in connection with deficient cellular autophagy. Blocking VimIF assembly by pharmacologic and genetic means also increases autophagic clearance of collagen type I. Furthermore, inhibition of expression of collagen type I by siRNA decreased invasiveness of fibroblasts. In a bleomycin injury model, enhancing autophagy in fibroblasts by an inhibitor of VimIF assembly, withaferin A (WFA), protected from fibrotic lung injury. Additionally, in 3D lung organoids, or pulmospheres, from patients with IPF, WFA reduced the invasiveness of lung fibroblasts in the majority of subjects tested. These studies provide insights into the functional role of vimentin, which regulates autophagy and restricts the invasiveness of lung fibroblasts.
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DOI: 10.1172/jci.insight.123253
PubMed: 30944258
PubMed Central: 6483650
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Ranu Surolia<affiliation><nlm:aff id="A1">Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine,</nlm:aff><wicri:noCountry code="subfield">Department of Medicine</wicri:noCountry></affiliation><affiliation><nlm:aff id="A1">Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine,</nlm:aff><wicri:noCountry code="subfield">Department of Medicine</wicri:noCountry></affiliation><affiliation><nlm:aff id="A1">Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine,</nlm:aff><wicri:noCountry code="subfield">Department of Medicine</wicri:noCountry></affiliation><affiliation><nlm:aff id="A1">Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine,</nlm:aff><wicri:noCountry code="subfield">Department of Medicine</wicri:noCountry></affiliation><affiliation><nlm:aff id="A1">Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine,</nlm:aff><wicri:noCountry code="subfield">Department of Medicine</wicri:noCountry></affiliation><affiliation><nlm:aff id="A1">Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine,</nlm:aff><wicri:noCountry code="subfield">Department of Medicine</wicri:noCountry></affiliation><affiliation><nlm:aff id="A1">Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine,</nlm:aff><wicri:noCountry code="subfield">Department of Medicine</wicri:noCountry></affiliation>Le document en format XML
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sort="Wang, Zheng" uniqKey="Wang Z" first="Zheng" last="Wang">Zheng Wang</name><affiliation><nlm:aff id="A1">Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine,</nlm:aff><wicri:noCountry code="subfield">Department of Medicine</wicri:noCountry></affiliation></author><author><name sortKey="Li, Huashi" sort="Li, Huashi" uniqKey="Li H" first="Huashi" last="Li">Huashi Li</name><affiliation><nlm:aff id="A1">Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine,</nlm:aff><wicri:noCountry code="subfield">Department of Medicine</wicri:noCountry></affiliation></author><author><name sortKey="Dsouza, Kevin" sort="Dsouza, Kevin" uniqKey="Dsouza K" first="Kevin" last="Dsouza">Kevin Dsouza</name><affiliation><nlm:aff id="A1">Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine,</nlm:aff><wicri:noCountry code="subfield">Department of Medicine</wicri:noCountry></affiliation></author><author><name sortKey="Thomas, Vinoy" sort="Thomas, Vinoy" uniqKey="Thomas V" first="Vinoy" last="Thomas">Vinoy Thomas</name><affiliation><nlm:aff wicri:cut=", and" id="A2">Department of Materials Science and Engineering</nlm:aff></affiliation></author><author><name sortKey="Mirov, Sergey" sort="Mirov, Sergey" uniqKey="Mirov S" first="Sergey" last="Mirov">Sergey Mirov</name><affiliation wicri:level="2"><nlm:aff id="A3">Department of Physics, University of Alabama at Birmingham (UAB), Birmingham, Alabama, USA.</nlm:aff><country xml:lang="fr" wicri:curation="lc">États-Unis</country><wicri:regionArea>Department of Physics, University of Alabama at Birmingham (UAB), Birmingham, Alabama</wicri:regionArea><placeName><region type="state">Alabama</region></placeName></affiliation></author><author><name sortKey="Perez Sala, Dolores" sort="Perez Sala, Dolores" uniqKey="Perez Sala D" first="Dolores" last="Pérez-Sala">Dolores Pérez-Sala</name><affiliation wicri:level="3"><nlm:aff id="A4">Department of Structural and Chemical and Biology, Centro de Investigaciones Biológicas, Consejo Superior de Investigaciones Científicas (CSIC), Madrid, Spain.</nlm:aff><country xml:lang="fr" wicri:curation="lc">Espagne</country><wicri:regionArea>Department of Structural and Chemical and Biology, Centro de Investigaciones Biológicas, Consejo Superior de Investigaciones Científicas (CSIC), Madrid</wicri:regionArea><placeName><settlement type="city">Madrid</settlement><region nuts="2" type="region">Communauté de Madrid</region></placeName></affiliation></author><author><name sortKey="Athar, Mohammad" sort="Athar, Mohammad" uniqKey="Athar M" first="Mohammad" last="Athar">Mohammad Athar</name><affiliation wicri:level="2"><nlm:aff id="A5">Department of Dermatology, UAB, Birmingham, Alabama, USA.</nlm:aff><country xml:lang="fr" wicri:curation="lc">États-Unis</country><wicri:regionArea>Department of Dermatology, UAB, Birmingham, Alabama</wicri:regionArea><placeName><region type="state">Alabama</region></placeName></affiliation></author><author><name sortKey="Thannickal, Victor J" sort="Thannickal, Victor J" uniqKey="Thannickal V" first="Victor J." last="Thannickal">Victor J. Thannickal</name><affiliation><nlm:aff id="A1">Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine,</nlm:aff><wicri:noCountry code="subfield">Department of Medicine</wicri:noCountry></affiliation></author><author><name sortKey="Antony, Veena B" sort="Antony, Veena B" uniqKey="Antony V" first="Veena B." last="Antony">Veena B. Antony</name><affiliation><nlm:aff id="A1">Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine,</nlm:aff><wicri:noCountry code="subfield">Department of Medicine</wicri:noCountry></affiliation></author></analytic><series><title level="j">JCI Insight</title><idno type="eISSN">2379-3708</idno><imprint><date when="????">????</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Idiopathic pulmonary fibrosis (IPF) is a progressive disease, with a median survival of 3–5 years following diagnosis. Lung remodeling by invasive fibroblasts is a hallmark of IPF. In this study, we demonstrate that inhibition of vimentin intermediate filaments (VimIFs) decreases the invasiveness of IPF fibroblasts and confers protection against fibrosis in a murine model of experimental lung injury. Increased expression and organization of VimIFs contribute to the invasive property of IPF fibroblasts in connection with deficient cellular autophagy. Blocking VimIF assembly by pharmacologic and genetic means also increases autophagic clearance of collagen type I. Furthermore, inhibition of expression of collagen type I by siRNA decreased invasiveness of fibroblasts. In a bleomycin injury model, enhancing autophagy in fibroblasts by an inhibitor of VimIF assembly, withaferin A (WFA), protected from fibrotic lung injury. Additionally, in 3D lung organoids, or pulmospheres, from patients with IPF, WFA reduced the invasiveness of lung fibroblasts in the majority of subjects tested. These studies provide insights into the functional role of vimentin, which regulates autophagy and restricts the invasiveness of lung fibroblasts.</p></div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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