Publikation:

Opposing effects of in vitro differentiated macrophages sub-type on epithelial wound healing

Lade...
Vorschaubild

Dateien

Gindele_2-13whjeffts4d13.pdf
Gindele_2-13whjeffts4d13.pdfGröße: 29.19 MBDownloads: 547

Datum

2017

Autor:innen

Gindele, Julia A.
Mang, Samuel
Pairet, Nicolas
Christ, Ingrid
Schymeinsky, Jürgen
Lamb, David J.

Herausgeber:innen

Kontakt

ISSN der Zeitschrift

Electronic ISSN

ISBN

Bibliografische Daten

Verlag

Schriftenreihe

Auflagebezeichnung

ArXiv-ID

Internationale Patentnummer

Link zur Lizenz

Angaben zur Forschungsförderung

Projekt

Open Access-Veröffentlichung
Open Access Gold
Core Facility der Universität Konstanz

Gesperrt bis

Titel in einer weiteren Sprache

Publikationstyp
Zeitschriftenartikel
Publikationsstatus
Published

Erschienen in

PLOS ONE. 2017, 12(9), e0184386. eISSN 1932-6203. Available under: doi: 10.1371/journal.pone.0184386

Zusammenfassung

Inappropriate repair responses to pulmonary epithelial injury have been linked to perturbation of epithelial barrier function and airway remodelling in a number of respiratory diseases, including chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis. We developed an in vitro mechanical scratch injury model in air-liquid interface differentiated primary human small airway epithelial cells that recapitulates many of the characteristics observed during epithelial wound injury in both human tissue and small animal models. Wound closure was initially associated with de-differentiation of the differentiated apical cells and rapid migration into the wound site, followed by proliferation of apical cells behind the wound edge, together with increases in FAK expression, fibronectin and reduction in PAI-1 which collectively facilitate cell motility and extracellular matrix deposition. Macrophages are intimately involved in wound repair so we sought to investigate the role of macrophage sub-types on this process in a novel primary human co-culture model. M1 macrophages promoted FAK expression and both M1 and M2 macrophages promoted epithelial de-differentiation. Interestingly, M2a macrophages inhibited both proliferation and fibronectin expression, possibly via the retinoic acid pathway, whereas M2b and M2c macrophages prevented fibronectin deposition, possibly via MMP expression. Collectively these data highlight the complex nature of epithelial wound closure, the differential impact of macrophage sub-types on this process, and the heterogenic and non-delineated function of these macrophages.

Zusammenfassung in einer weiteren Sprache

Fachgebiet (DDC)
570 Biowissenschaften, Biologie

Schlagwörter

Konferenz

Rezension
undefined / . - undefined, undefined

Forschungsvorhaben

Organisationseinheiten

Zeitschriftenheft

Zugehörige Datensätze in KOPS

Zitieren

ISO 690GINDELE, Julia A., Samuel MANG, Nicolas PAIRET, Ingrid CHRIST, Florian GANTNER, Jürgen SCHYMEINSKY, David J. LAMB, 2017. Opposing effects of in vitro differentiated macrophages sub-type on epithelial wound healing. In: PLOS ONE. 2017, 12(9), e0184386. eISSN 1932-6203. Available under: doi: 10.1371/journal.pone.0184386
BibTex
@article{Gindele2017Oppos-40621,
  year={2017},
  doi={10.1371/journal.pone.0184386},
  title={Opposing effects of in vitro differentiated macrophages sub-type on epithelial wound healing},
  number={9},
  volume={12},
  journal={PLOS ONE},
  author={Gindele, Julia A. and Mang, Samuel and Pairet, Nicolas and Christ, Ingrid and Gantner, Florian and Schymeinsky, Jürgen and Lamb, David J.},
  note={DOAJ, 15.11.2017 fn Article Number: e0184386}
}
RDF
<rdf:RDF
    xmlns:dcterms="http://purl.org/dc/terms/"
    xmlns:dc="http://purl.org/dc/elements/1.1/"
    xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#"
    xmlns:bibo="http://purl.org/ontology/bibo/"
    xmlns:dspace="http://digital-repositories.org/ontologies/dspace/0.1.0#"
    xmlns:foaf="http://xmlns.com/foaf/0.1/"
    xmlns:void="http://rdfs.org/ns/void#"
    xmlns:xsd="http://www.w3.org/2001/XMLSchema#" > 
  <rdf:Description rdf:about="https://kops.uni-konstanz.de/server/rdf/resource/123456789/40621">
    <dcterms:issued>2017</dcterms:issued>
    <dc:creator>Mang, Samuel</dc:creator>
    <dc:creator>Gindele, Julia A.</dc:creator>
    <dcterms:isPartOf rdf:resource="https://kops.uni-konstanz.de/server/rdf/resource/123456789/28"/>
    <dc:contributor>Mang, Samuel</dc:contributor>
    <dc:creator>Schymeinsky, Jürgen</dc:creator>
    <foaf:homepage rdf:resource="http://localhost:8080/"/>
    <dc:creator>Gantner, Florian</dc:creator>
    <dc:creator>Lamb, David J.</dc:creator>
    <dspace:hasBitstream rdf:resource="https://kops.uni-konstanz.de/bitstream/123456789/40621/1/Gindele_2-13whjeffts4d13.pdf"/>
    <dc:contributor>Gindele, Julia A.</dc:contributor>
    <dc:contributor>Lamb, David J.</dc:contributor>
    <dcterms:abstract xml:lang="eng">Inappropriate repair responses to pulmonary epithelial injury have been linked to perturbation of epithelial barrier function and airway remodelling in a number of respiratory diseases, including chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis. We developed an in vitro mechanical scratch injury model in air-liquid interface differentiated primary human small airway epithelial cells that recapitulates many of the characteristics observed during epithelial wound injury in both human tissue and small animal models. Wound closure was initially associated with de-differentiation of the differentiated apical cells and rapid migration into the wound site, followed by proliferation of apical cells behind the wound edge, together with increases in FAK expression, fibronectin and reduction in PAI-1 which collectively facilitate cell motility and extracellular matrix deposition. Macrophages are intimately involved in wound repair so we sought to investigate the role of macrophage sub-types on this process in a novel primary human co-culture model. M1 macrophages promoted FAK expression and both M1 and M2 macrophages promoted epithelial de-differentiation. Interestingly, M2a macrophages inhibited both proliferation and fibronectin expression, possibly via the retinoic acid pathway, whereas M2b and M2c macrophages prevented fibronectin deposition, possibly via MMP expression. Collectively these data highlight the complex nature of epithelial wound closure, the differential impact of macrophage sub-types on this process, and the heterogenic and non-delineated function of these macrophages.</dcterms:abstract>
    <bibo:uri rdf:resource="https://kops.uni-konstanz.de/handle/123456789/40621"/>
    <dc:rights>Attribution 4.0 International</dc:rights>
    <dc:creator>Christ, Ingrid</dc:creator>
    <dc:language>eng</dc:language>
    <dc:date rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2017-11-15T08:51:26Z</dc:date>
    <dcterms:hasPart rdf:resource="https://kops.uni-konstanz.de/bitstream/123456789/40621/1/Gindele_2-13whjeffts4d13.pdf"/>
    <dc:contributor>Pairet, Nicolas</dc:contributor>
    <dspace:isPartOfCollection rdf:resource="https://kops.uni-konstanz.de/server/rdf/resource/123456789/28"/>
    <dc:contributor>Christ, Ingrid</dc:contributor>
    <dcterms:title>Opposing effects of in vitro differentiated macrophages sub-type on epithelial wound healing</dcterms:title>
    <dcterms:rights rdf:resource="http://creativecommons.org/licenses/by/4.0/"/>
    <void:sparqlEndpoint rdf:resource="http://localhost/fuseki/dspace/sparql"/>
    <dc:contributor>Gantner, Florian</dc:contributor>
    <dc:contributor>Schymeinsky, Jürgen</dc:contributor>
    <dc:creator>Pairet, Nicolas</dc:creator>
    <dcterms:available rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2017-11-15T08:51:26Z</dcterms:available>
  </rdf:Description>
</rdf:RDF>

Interner Vermerk

xmlui.Submission.submit.DescribeStep.inputForms.label.kops_note_fromSubmitter

Kontakt
URL der Originalveröffentl.

Prüfdatum der URL

Prüfungsdatum der Dissertation

Finanzierungsart

Kommentar zur Publikation

DOAJ, 15.11.2017 fn
Allianzlizenz
Corresponding Authors der Uni Konstanz vorhanden
Internationale Co-Autor:innen
Universitätsbibliographie
Ja
Begutachtet
Diese Publikation teilen