Kallikrein-related peptidase 5 contributes to the remodeling and repair of bronchial epithelium.
Aged
Airway Remodeling
Antigens, CD
/ genetics
Bronchi
/ metabolism
Cadherins
/ genetics
Case-Control Studies
Cells, Cultured
Epithelial Cells
/ metabolism
Epithelial-Mesenchymal Transition
Female
Humans
Kallikreins
/ genetics
Lung Neoplasms
/ metabolism
Male
Middle Aged
Pulmonary Disease, Chronic Obstructive
/ metabolism
Signal Transduction
COPD
airway repair
bronchial remodeling
epithelial-mesenchymal transition
kallikrein-related peptidase 5
Journal
FASEB journal : official publication of the Federation of American Societies for Experimental Biology
ISSN: 1530-6860
Titre abrégé: FASEB J
Pays: United States
ID NLM: 8804484
Informations de publication
Date de publication:
10 2021
10 2021
Historique:
revised:
28
06
2021
received:
05
12
2020
accepted:
21
07
2021
pubmed:
29
9
2021
medline:
21
10
2021
entrez:
28
9
2021
Statut:
ppublish
Résumé
Inflammation, oxidative stress, and protease/protease inhibitor imbalance with excessive production of proteases are factors associated with pathogenesis of the chronic obstructive pulmonary disease (COPD). In this study, we report that kallikrein-related peptidase 5 (KLK5) is a crucial protease involved in extracellular matrix (ECM) remodeling and bronchial epithelial repair after injury. First, we showed that KLK5 degrades the basal layer formed by culture of primary bronchial epithelial cells from COPD or non-COPD patients. Also, exogenous KLK5 acted differently on BEAS-2B cells already engaged in epithelial-to-mesenchymal transition (EMT) or on 16HBE 14o- cells harboring epithelial characteristics. Indeed, by inducing EMT, KLK5 reduced BEAS-2B cell adherence to the ECM. This effect, neutralized by tissue factor pathway inhibitor 2, a kunitz-type serine protease inhibitor, was due to a direct proteolytic activity of KLK5 on E-cadherin, β-catenin, fibronectin, and α5β1 integrin. Thus, KLK5 may strengthen EMT mechanisms and promote the migration of cells by activating the mitogen-activated protein kinase signaling pathway required for this function. In contrast, knockdown of endogenous KLK5 in 16HBE14o- cells, accelerated wound healing repair after injury, and exogenous KLK5 addition delayed the closure repair. These data suggest that among proteases, KLK5 could play a critical role in airway remodeling events associated with COPD during exposure of the pulmonary epithelium to inhaled irritants or smoking and the inflammation process.
Identifiants
pubmed: 34582061
doi: 10.1096/fj.202002649R
doi:
Substances chimiques
Antigens, CD
0
CDH1 protein, human
0
Cadherins
0
KLK5 protein, human
EC 3.4.21.-
Kallikreins
EC 3.4.21.-
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e21838Informations de copyright
© 2021 Federation of American Societies for Experimental Biology.
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