Mesenchymal WNT-5A/5B Signaling Represses Lung Alveolar Epithelial Progenitors.
Aging
/ metabolism
Alveolar Epithelial Cells
/ cytology
Animals
Cell Differentiation
Cell Line
Cell Proliferation
Coculture Techniques
Female
Fibroblasts
/ cytology
Humans
Male
Mice
Organoids
/ cytology
Pulmonary Disease, Chronic Obstructive
/ metabolism
Stem Cells
/ cytology
Up-Regulation
Wnt Proteins
/ metabolism
Wnt Signaling Pathway
Wnt-5a Protein
/ metabolism
WNT signaling pathway
WNT-5A
WNT-5B
alveolar repair
chronic obstructive pulmonary disease (COPD)
lung organoids
precision-cut-lung slices (PCLS)
Journal
Cells
ISSN: 2073-4409
Titre abrégé: Cells
Pays: Switzerland
ID NLM: 101600052
Informations de publication
Date de publication:
25 09 2019
25 09 2019
Historique:
received:
29
08
2019
revised:
17
09
2019
accepted:
25
09
2019
entrez:
28
9
2019
pubmed:
29
9
2019
medline:
17
6
2020
Statut:
epublish
Résumé
Chronic obstructive pulmonary disease (COPD) represents a worldwide concern with high morbidity and mortality, and is believed to be associated with accelerated ageing of the lung. Alveolar abnormalities leading to emphysema are a key characteristic of COPD. Pulmonary alveolar epithelial type 2 cells (AT2) produce surfactant and function as progenitors for type 1 cells. Increasing evidence shows elevated WNT-5A/B expression in ageing and in COPD that may contribute to the disease process. However, supportive roles for WNT-5A/B in lung regeneration were also reported in different studies. Thus, we explored the role of WNT-5A/B on alveolar epithelial progenitors (AEPs) in more detail. We established a Precision-Cut-Lung Slices (PCLS) model and a lung organoid model by co-culturing epithelial cells (EpCAM
Identifiants
pubmed: 31557955
pii: cells8101147
doi: 10.3390/cells8101147
pmc: PMC6829372
pii:
doi:
Substances chimiques
Wnt Proteins
0
Wnt-5a Protein
0
Wnt5a protein, mouse
0
Wnt5b protein, mouse
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NHLBI NIH HHS
ID : R01 HL141380
Pays : United States
Déclaration de conflit d'intérêts
The authors declare no conflict of interest.
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