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Mast cell tryptase enhances wound healing by promoting migration in human bronchial epithelial cells

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Mogren, Sofia ; Berlin, Frida ; Ramu, Sangeetha ; Sverrild, Asger ; Porsbjerg, Celeste ; Uller, Lena ; Andersson, Cecilia K. / Mast cell tryptase enhances wound healing by promoting migration in human bronchial epithelial cells. I: Cell adhesion & migration. 2021 ; Bind 15, Nr. 1. s. 202-214.

Bibtex

@article{56c0831484194e7eabe5c33859ce5e0c,
title = "Mast cell tryptase enhances wound healing by promoting migration in human bronchial epithelial cells",
abstract = "Epithelial damage and increase of intraepithelial mast cells (MC) are characteristics of asthma. The role of MC mediator tryptase and the protease-activated receptor-2 (PAR2) on epithelial wound healing is not fully investigated. Stimulation of bronchial epithelial cells (BECs) with tryptase promoted gap closure, migration and cellular speed compared to controls. Stimulated BECs had higher expression of migration marker CD151 compared to controls. Proliferation marker KI67 was upregulated in tryptase-stimulated BECs compared to controls. Treatment with PAR2 antagonist I-191 reduced gap closure, migration and cell speed compared to BECs stimulated with tryptase. We found that tryptase enhances epithelial wound healing by increased migration and proliferation, which is in part regulated via PAR2. Our data suggest that tryptase might be beneficial in tissue repair under baseline conditions. However, in a pathological context such as asthma with increased numbers of activated MCs, it might lead to epithelial remodeling and loss of function.",
keywords = "epithelial cells, Mast cell, protease activated receptor 2, tryptase, wound healing",
author = "Sofia Mogren and Frida Berlin and Sangeetha Ramu and Asger Sverrild and Celeste Porsbjerg and Lena Uller and Andersson, {Cecilia K}",
year = "2021",
month = dec,
doi = "10.1080/19336918.2021.1950594",
language = "English",
volume = "15",
pages = "202--214",
journal = "Cell adhesion & migration",
issn = "1933-6918",
publisher = "Landes Bioscience",
number = "1",

}

RIS

TY - JOUR

T1 - Mast cell tryptase enhances wound healing by promoting migration in human bronchial epithelial cells

AU - Mogren, Sofia

AU - Berlin, Frida

AU - Ramu, Sangeetha

AU - Sverrild, Asger

AU - Porsbjerg, Celeste

AU - Uller, Lena

AU - Andersson, Cecilia K

PY - 2021/12

Y1 - 2021/12

N2 - Epithelial damage and increase of intraepithelial mast cells (MC) are characteristics of asthma. The role of MC mediator tryptase and the protease-activated receptor-2 (PAR2) on epithelial wound healing is not fully investigated. Stimulation of bronchial epithelial cells (BECs) with tryptase promoted gap closure, migration and cellular speed compared to controls. Stimulated BECs had higher expression of migration marker CD151 compared to controls. Proliferation marker KI67 was upregulated in tryptase-stimulated BECs compared to controls. Treatment with PAR2 antagonist I-191 reduced gap closure, migration and cell speed compared to BECs stimulated with tryptase. We found that tryptase enhances epithelial wound healing by increased migration and proliferation, which is in part regulated via PAR2. Our data suggest that tryptase might be beneficial in tissue repair under baseline conditions. However, in a pathological context such as asthma with increased numbers of activated MCs, it might lead to epithelial remodeling and loss of function.

AB - Epithelial damage and increase of intraepithelial mast cells (MC) are characteristics of asthma. The role of MC mediator tryptase and the protease-activated receptor-2 (PAR2) on epithelial wound healing is not fully investigated. Stimulation of bronchial epithelial cells (BECs) with tryptase promoted gap closure, migration and cellular speed compared to controls. Stimulated BECs had higher expression of migration marker CD151 compared to controls. Proliferation marker KI67 was upregulated in tryptase-stimulated BECs compared to controls. Treatment with PAR2 antagonist I-191 reduced gap closure, migration and cell speed compared to BECs stimulated with tryptase. We found that tryptase enhances epithelial wound healing by increased migration and proliferation, which is in part regulated via PAR2. Our data suggest that tryptase might be beneficial in tissue repair under baseline conditions. However, in a pathological context such as asthma with increased numbers of activated MCs, it might lead to epithelial remodeling and loss of function.

KW - epithelial cells

KW - Mast cell

KW - protease activated receptor 2

KW - tryptase

KW - wound healing

UR - http://www.scopus.com/inward/record.url?scp=85111119719&partnerID=8YFLogxK

U2 - 10.1080/19336918.2021.1950594

DO - 10.1080/19336918.2021.1950594

M3 - Journal article

C2 - 34308764

VL - 15

SP - 202

EP - 214

JO - Cell adhesion & migration

JF - Cell adhesion & migration

SN - 1933-6918

IS - 1

ER -

ID: 66957163