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

Sofia Mogren; Frida Berlin; Sangeetha Ramu; Asger Sverrild; Celeste Porsbjerg; Lena Uller; Cecilia Andersson

doi:10.1080/19336918.2021.1950594

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

Sofia Mogren, Frida Berlin, Sangeetha Ramu, Asger Sverrild, Celeste Porsbjerg, Lena Uller, Cecilia Andersson

Research output: Contribution to journal › Article › peer-review

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.

Original language	English
Pages (from-to)	202-214
Journal	Cell Adhesion and Migration
Volume	15
Issue number	1
DOIs	https://doi.org/10.1080/19336918.2021.1950594
Publication status	Published - 2021

Subject classification (UKÄ)

Cell and Molecular Biology
Respiratory Medicine and Allergy

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10.1080/19336918.2021.1950594Licence: CC BY

2 Doctoral Thesis (compilation)

Mastering Repair: How Mast Cells and Their Mediators Shape Respiratory Health and Disease
Mogren, S., 2024, Lund: Lund University, Faculty of Medicine. 66 p.
Research output: Thesis › Doctoral Thesis (compilation)

Open Access
File
Mast Cell-Mediated Orchestration of Airway Epithelial Responses in Chronic Respiratory Diseases
Berlin, F., 2023, Lund: Lund University, Faculty of Medicine. 64 p.
Research output: Thesis › Doctoral Thesis (compilation)

Open Access
File

Cite this

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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.",

author = "Sofia Mogren and Frida Berlin and Sangeetha Ramu and Asger Sverrild and Celeste Porsbjerg and Lena Uller and Cecilia Andersson",

year = "2021",

doi = "10.1080/19336918.2021.1950594",

language = "English",

volume = "15",

pages = "202--214",

journal = "Cell Adhesion and Migration",

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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

PY - 2021

Y1 - 2021

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.

U2 - 10.1080/19336918.2021.1950594

DO - 10.1080/19336918.2021.1950594

M3 - Article

C2 - 34308764

SN - 1933-6918

VL - 15

SP - 202

EP - 214

JO - Cell Adhesion and Migration

JF - Cell Adhesion and Migration

IS - 1

ER -

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

Abstract

Subject classification (UKÄ)

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Research output

Mastering Repair: How Mast Cells and Their Mediators Shape Respiratory Health and Disease

Mast Cell-Mediated Orchestration of Airway Epithelial Responses in Chronic Respiratory Diseases

Cite this