Glutaredoxin deficiency promotes activation of the transforming growth factor beta pathway in airway epithelial cells, in association with fibrotic airway remodeling.
Identifieur interne : 000067 ( Main/Exploration ); précédent : 000066; suivant : 000068Glutaredoxin deficiency promotes activation of the transforming growth factor beta pathway in airway epithelial cells, in association with fibrotic airway remodeling.
Auteurs : Shi B. Chia [États-Unis] ; James D. Nolin [États-Unis] ; Reem Aboushousha [États-Unis] ; Cuixia Erikson [États-Unis] ; Charles G. Irvin [États-Unis] ; Matthew E. Poynter [États-Unis] ; Jos Van Der Velden [États-Unis] ; Douglas J. Taatjes [États-Unis] ; Albert Van Der Vliet [États-Unis] ; Vikas Anathy [États-Unis] ; Yvonne M W. Janssen-Heininger [États-Unis]Source :
- Redox biology [ 2213-2317 ] ; 2020.
Abstract
S-glutathionylation of reactive protein cysteines is a post-translational event that plays a critical role in transducing signals from oxidants into biological responses. S-glutathionylation can be reversed by the deglutathionylating enzyme glutaredoxin (GLRX). We have previously demonstrated that ablation of Glrx sensitizes mice to the development of parenchymal lung fibrosis(1). It remains unclear whether GLRX also controls airway fibrosis, a clinical feature relevant to asthma and chronic obstructive pulmonary disease, and whether GLRX controls the biology of airway epithelial cells, which have been implicated in the pathophysiology of these diseases. In the present study we utilized a house dust mite (HDM) model of allergic airway disease in wild type (WT) and Glrx-/- mice on a C57BL/6 background prone to develop airway fibrosis, and tracheal basal stem cells derived from WT mice, global Glrx-/- mice, or bi-transgenic mice allowing conditional ablation of the Glrx gene. Herein we show that absence of Glrx led to enhanced HDM-induced collagen deposition, elevated levels of transforming growth factor beta 1 (TGFB1) in the bronchoalveolar lavage, and resulted in increases in airway hyperresponsiveness. Airway epithelial cells isolated from Glrx-/- mice or following conditional ablation of Glrx showed spontaneous increases in secretion of TGFB1. Glrx-/- basal cells also showed spontaneous TGFB pathway activation, in association with increased expression of mesenchymal genes, including collagen 1a1 and fibronectin. Overall, these findings suggest that GLRX regulates airway fibrosis via a mechanism(s) that involve the plasticity of basal cells, the stem cells of the airways.
DOI: 10.1016/j.redox.2020.101720
PubMed: 32971362
PubMed Central: PMC7509797
Affiliations:
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Janssen-Heininger</name><affiliation wicri:level="1"><nlm:affiliation>Department of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, VT, 05405, USA. 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Chia</name><affiliation wicri:level="1"><nlm:affiliation>Department of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, VT, 05405, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, VT, 05405</wicri:regionArea><wicri:noRegion>05405</wicri:noRegion></affiliation></author><author><name sortKey="Nolin, James D" sort="Nolin, James D" uniqKey="Nolin J" first="James D" last="Nolin">James D. Nolin</name><affiliation wicri:level="1"><nlm:affiliation>Department of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, VT, 05405, USA; Center for Genes, Environment and Health, National Jewish Health, Denver, CO, 80206, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, VT, 05405, USA; Center for Genes, Environment and Health, National Jewish Health, Denver, CO, 80206</wicri:regionArea><wicri:noRegion>80206</wicri:noRegion></affiliation></author><author><name sortKey="Aboushousha, Reem" sort="Aboushousha, Reem" uniqKey="Aboushousha R" first="Reem" last="Aboushousha">Reem Aboushousha</name><affiliation wicri:level="1"><nlm:affiliation>Department of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, VT, 05405, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, VT, 05405</wicri:regionArea><wicri:noRegion>05405</wicri:noRegion></affiliation></author><author><name sortKey="Erikson, Cuixia" sort="Erikson, Cuixia" uniqKey="Erikson C" first="Cuixia" last="Erikson">Cuixia Erikson</name><affiliation wicri:level="1"><nlm:affiliation>Department of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, VT, 05405, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, VT, 05405</wicri:regionArea><wicri:noRegion>05405</wicri:noRegion></affiliation></author><author><name sortKey="Irvin, Charles G" sort="Irvin, Charles G" uniqKey="Irvin C" first="Charles G" last="Irvin">Charles G. Irvin</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medicine, University of Vermont College of Medicine, Burlington, VT, 05405, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, University of Vermont College of Medicine, Burlington, VT, 05405</wicri:regionArea><wicri:noRegion>05405</wicri:noRegion></affiliation></author><author><name sortKey="Poynter, Matthew E" sort="Poynter, Matthew E" uniqKey="Poynter M" first="Matthew E" last="Poynter">Matthew E. Poynter</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medicine, University of Vermont College of Medicine, Burlington, VT, 05405, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, University of Vermont College of Medicine, Burlington, VT, 05405</wicri:regionArea><wicri:noRegion>05405</wicri:noRegion></affiliation></author><author><name sortKey="Van Der Velden, Jos" sort="Van Der Velden, Jos" uniqKey="Van Der Velden J" first="Jos" last="Van Der Velden">Jos Van Der Velden</name><affiliation wicri:level="1"><nlm:affiliation>Department of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, VT, 05405, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, VT, 05405</wicri:regionArea><wicri:noRegion>05405</wicri:noRegion></affiliation></author><author><name sortKey="Taatjes, Douglas J" sort="Taatjes, Douglas J" uniqKey="Taatjes D" first="Douglas J" last="Taatjes">Douglas J. Taatjes</name><affiliation wicri:level="1"><nlm:affiliation>Department of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, VT, 05405, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, VT, 05405</wicri:regionArea><wicri:noRegion>05405</wicri:noRegion></affiliation></author><author><name sortKey="Van Der Vliet, Albert" sort="Van Der Vliet, Albert" uniqKey="Van Der Vliet A" first="Albert" last="Van Der Vliet">Albert Van Der Vliet</name><affiliation wicri:level="1"><nlm:affiliation>Department of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, VT, 05405, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, VT, 05405</wicri:regionArea><wicri:noRegion>05405</wicri:noRegion></affiliation></author><author><name sortKey="Anathy, Vikas" sort="Anathy, Vikas" uniqKey="Anathy V" first="Vikas" last="Anathy">Vikas Anathy</name><affiliation wicri:level="1"><nlm:affiliation>Department of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, VT, 05405, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, VT, 05405</wicri:regionArea><wicri:noRegion>05405</wicri:noRegion></affiliation></author><author><name sortKey="Janssen Heininger, Yvonne M W" sort="Janssen Heininger, Yvonne M W" uniqKey="Janssen Heininger Y" first="Yvonne M W" last="Janssen-Heininger">Yvonne M W. Janssen-Heininger</name><affiliation wicri:level="1"><nlm:affiliation>Department of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, VT, 05405, USA. Electronic address: Yvonne.janssen@uvm.edu.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, VT, 05405</wicri:regionArea><wicri:noRegion>05405</wicri:noRegion></affiliation></author></analytic><series><title level="j">Redox biology</title><idno type="eISSN">2213-2317</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">S-glutathionylation of reactive protein cysteines is a post-translational event that plays a critical role in transducing signals from oxidants into biological responses. S-glutathionylation can be reversed by the deglutathionylating enzyme glutaredoxin (GLRX). We have previously demonstrated that ablation of Glrx sensitizes mice to the development of parenchymal lung fibrosis(1). It remains unclear whether GLRX also controls airway fibrosis, a clinical feature relevant to asthma and chronic obstructive pulmonary disease, and whether GLRX controls the biology of airway epithelial cells, which have been implicated in the pathophysiology of these diseases. In the present study we utilized a house dust mite (HDM) model of allergic airway disease in wild type (WT) and Glrx<sup>-/-</sup> mice on a C57BL/6 background prone to develop airway fibrosis, and tracheal basal stem cells derived from WT mice, global Glrx<sup>-/-</sup> mice, or bi-transgenic mice allowing conditional ablation of the Glrx gene. Herein we show that absence of Glrx led to enhanced HDM-induced collagen deposition, elevated levels of transforming growth factor beta 1 (TGFB1) in the bronchoalveolar lavage, and resulted in increases in airway hyperresponsiveness. Airway epithelial cells isolated from Glrx<sup>-/-</sup> mice or following conditional ablation of Glrx showed spontaneous increases in secretion of TGFB1. Glrx<sup>-/-</sup> basal cells also showed spontaneous TGFB pathway activation, in association with increased expression of mesenchymal genes, including collagen 1a1 and fibronectin. Overall, these findings suggest that GLRX regulates airway fibrosis via a mechanism(s) that involve the plasticity of basal cells, the stem cells of the airways.</div></front></TEI><pubmed><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">32971362</PMID><DateRevised><Year>2020</Year><Month>11</Month><Day>03</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">2213-2317</ISSN><JournalIssue CitedMedium="Internet"><Volume>37</Volume><PubDate><Year>2020</Year><Month>Sep</Month><Day>14</Day></PubDate></JournalIssue><Title>Redox biology</Title><ISOAbbreviation>Redox Biol</ISOAbbreviation></Journal><ArticleTitle>Glutaredoxin deficiency promotes activation of the transforming growth factor beta pathway in airway epithelial cells, in association with fibrotic airway remodeling.</ArticleTitle><Pagination><MedlinePgn>101720</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S2213-2317(20)30925-3</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.redox.2020.101720</ELocationID><Abstract><AbstractText>S-glutathionylation of reactive protein cysteines is a post-translational event that plays a critical role in transducing signals from oxidants into biological responses. S-glutathionylation can be reversed by the deglutathionylating enzyme glutaredoxin (GLRX). We have previously demonstrated that ablation of Glrx sensitizes mice to the development of parenchymal lung fibrosis(1). It remains unclear whether GLRX also controls airway fibrosis, a clinical feature relevant to asthma and chronic obstructive pulmonary disease, and whether GLRX controls the biology of airway epithelial cells, which have been implicated in the pathophysiology of these diseases. In the present study we utilized a house dust mite (HDM) model of allergic airway disease in wild type (WT) and Glrx<sup>-/-</sup> mice on a C57BL/6 background prone to develop airway fibrosis, and tracheal basal stem cells derived from WT mice, global Glrx<sup>-/-</sup> mice, or bi-transgenic mice allowing conditional ablation of the Glrx gene. Herein we show that absence of Glrx led to enhanced HDM-induced collagen deposition, elevated levels of transforming growth factor beta 1 (TGFB1) in the bronchoalveolar lavage, and resulted in increases in airway hyperresponsiveness. Airway epithelial cells isolated from Glrx<sup>-/-</sup> mice or following conditional ablation of Glrx showed spontaneous increases in secretion of TGFB1. Glrx<sup>-/-</sup> basal cells also showed spontaneous TGFB pathway activation, in association with increased expression of mesenchymal genes, including collagen 1a1 and fibronectin. Overall, these findings suggest that GLRX regulates airway fibrosis via a mechanism(s) that involve the plasticity of basal cells, the stem cells of the airways.</AbstractText><CopyrightInformation>Published by Elsevier B.V.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Chia</LastName><ForeName>Shi B</ForeName><Initials>SB</Initials><AffiliationInfo><Affiliation>Department of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, VT, 05405, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nolin</LastName><ForeName>James D</ForeName><Initials>JD</Initials><AffiliationInfo><Affiliation>Department of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, VT, 05405, USA; Center for Genes, Environment and Health, National Jewish Health, Denver, CO, 80206, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Aboushousha</LastName><ForeName>Reem</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, VT, 05405, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Erikson</LastName><ForeName>Cuixia</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, VT, 05405, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Irvin</LastName><ForeName>Charles G</ForeName><Initials>CG</Initials><AffiliationInfo><Affiliation>Department of Medicine, University of Vermont College of Medicine, Burlington, VT, 05405, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Poynter</LastName><ForeName>Matthew E</ForeName><Initials>ME</Initials><AffiliationInfo><Affiliation>Department of Medicine, University of Vermont College of Medicine, Burlington, VT, 05405, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>van der Velden</LastName><ForeName>Jos</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, VT, 05405, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Taatjes</LastName><ForeName>Douglas J</ForeName><Initials>DJ</Initials><AffiliationInfo><Affiliation>Department of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, VT, 05405, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>van der Vliet</LastName><ForeName>Albert</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, VT, 05405, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Anathy</LastName><ForeName>Vikas</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>Department of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, VT, 05405, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Janssen-Heininger</LastName><ForeName>Yvonne M W</ForeName><Initials>YMW</Initials><AffiliationInfo><Affiliation>Department of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, VT, 05405, USA. Electronic address: Yvonne.janssen@uvm.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R35 HL135828</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>09</Month><Day>14</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Redox Biol</MedlineTA><NlmUniqueID>101605639</NlmUniqueID><ISSNLinking>2213-2317</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Asthma</Keyword><Keyword MajorTopicYN="N">Basal cells</Keyword><Keyword MajorTopicYN="N">COPD</Keyword><Keyword MajorTopicYN="N">Fibrosis</Keyword><Keyword MajorTopicYN="N">S-glutathionylation</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2020</Year><Month>04</Month><Day>26</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2020</Year><Month>09</Month><Day>02</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2020</Year><Month>09</Month><Day>11</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>9</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>9</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>9</Month><Day>24</Day><Hour>20</Hour><Minute>12</Minute></PubMedPubDate></History><PublicationStatus>aheadofprint</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32971362</ArticleId><ArticleId IdType="pii">S2213-2317(20)30925-3</ArticleId><ArticleId IdType="doi">10.1016/j.redox.2020.101720</ArticleId><ArticleId IdType="pmc">PMC7509797</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country></list><tree><country name="États-Unis"><noRegion><name sortKey="Chia, Shi B" sort="Chia, Shi B" uniqKey="Chia S" first="Shi B" last="Chia">Shi B. Chia</name></noRegion><name sortKey="Aboushousha, Reem" sort="Aboushousha, Reem" uniqKey="Aboushousha R" first="Reem" last="Aboushousha">Reem Aboushousha</name><name sortKey="Anathy, Vikas" sort="Anathy, Vikas" uniqKey="Anathy V" first="Vikas" last="Anathy">Vikas Anathy</name><name sortKey="Erikson, Cuixia" sort="Erikson, Cuixia" uniqKey="Erikson C" first="Cuixia" last="Erikson">Cuixia Erikson</name><name sortKey="Irvin, Charles G" sort="Irvin, Charles G" uniqKey="Irvin C" first="Charles G" last="Irvin">Charles G. Irvin</name><name sortKey="Janssen Heininger, Yvonne M W" sort="Janssen Heininger, Yvonne M W" uniqKey="Janssen Heininger Y" first="Yvonne M W" last="Janssen-Heininger">Yvonne M W. Janssen-Heininger</name><name sortKey="Nolin, James D" sort="Nolin, James D" uniqKey="Nolin J" first="James D" last="Nolin">James D. Nolin</name><name sortKey="Poynter, Matthew E" sort="Poynter, Matthew E" uniqKey="Poynter M" first="Matthew E" last="Poynter">Matthew E. Poynter</name><name sortKey="Taatjes, Douglas J" sort="Taatjes, Douglas J" uniqKey="Taatjes D" first="Douglas J" last="Taatjes">Douglas J. Taatjes</name><name sortKey="Van Der Velden, Jos" sort="Van Der Velden, Jos" uniqKey="Van Der Velden J" first="Jos" last="Van Der Velden">Jos Van Der Velden</name><name sortKey="Van Der Vliet, Albert" sort="Van Der Vliet, Albert" uniqKey="Van Der Vliet A" first="Albert" last="Van Der Vliet">Albert Van Der Vliet</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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