DOCK2 Promotes Pleural Fibrosis by Modulating Mesothelial to Mesenchymal Transition.
Animals
Antibiotics, Antineoplastic
/ toxicity
Bleomycin
/ toxicity
Disease Models, Animal
Epithelial-Mesenchymal Transition
Epithelium
/ metabolism
Fibrosis
/ chemically induced
GTPase-Activating Proteins
/ genetics
Guanine Nucleotide Exchange Factors
/ genetics
Humans
Mice
Mice, Inbred C57BL
Pleura
/ metabolism
Pleurisy
/ chemically induced
Signal Transduction
Transforming Growth Factor beta
/ genetics
DOCK2
TGF-β
lung
mesothelial to mesenchymal transition
pleural fibrosis
Journal
American journal of respiratory cell and molecular biology
ISSN: 1535-4989
Titre abrégé: Am J Respir Cell Mol Biol
Pays: United States
ID NLM: 8917225
Informations de publication
Date de publication:
02 2022
02 2022
Historique:
pubmed:
29
10
2021
medline:
15
2
2022
entrez:
28
10
2021
Statut:
ppublish
Résumé
Mesothelial to mesenchymal transition (MesoMT) is one of the crucial mechanisms underlying pleural fibrosis, which results in restrictive lung disease. DOCK2 (dedicator of cytokinesis 2) plays important roles in immune functions; however, its role in pleural fibrosis, particularly MesoMT, remains unknown. We found that amounts of DOCK2 and the MesoMT marker α-SMA (α-smooth muscle actin) were significantly elevated and colocalized in the thickened pleura of patients with nonspecific pleuritis, suggesting the involvement of DOCK2 in the pathogenesis of MesoMT and pleural fibrosis. Likewise, data from three different pleural fibrosis models (TGF-β [transforming growth factor-β], carbon black/bleomycin, and streptococcal empyema) consistently demonstrated DOCK2 upregulation and its colocalization with α-SMA in the pleura. In addition, induced DOCK2 colocalized with the mesothelial marker calretinin, implicating DOCK2 in the regulation of MesoMT. Our
Identifiants
pubmed: 34710342
doi: 10.1165/rcmb.2021-0175OC
pmc: PMC8845130
doi:
Substances chimiques
Antibiotics, Antineoplastic
0
DOCK2 protein, mouse
0
GTPase-Activating Proteins
0
Guanine Nucleotide Exchange Factors
0
Transforming Growth Factor beta
0
Bleomycin
11056-06-7
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
Pagination
171-182Subventions
Organisme : NHLBI NIH HHS
ID : R01 HL130133
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL142853
Pays : United States
Organisme : NHLBI NIH HHS
ID : K99 HL141583
Pays : United States
Organisme : NHLBI NIH HHS
ID : R00 HL141583
Pays : United States
Organisme : Foundation for the National Institutes of Health
ID : HL141583
Commentaires et corrections
Type : CommentIn
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