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肥大细胞类胰蛋白酶通过促进人支气管上皮细胞迁移来增强伤口愈合。

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

机构信息

Department of Experimental Medical Science, Lund University, Lund, Sweden.

Department of Respiratory Medicine, Bispebjerg and Frederiksberg Hospital, Copenhagen, Denmark.

出版信息

Cell Adh Migr. 2021 Dec;15(1):202-214. doi: 10.1080/19336918.2021.1950594.

DOI:10.1080/19336918.2021.1950594
PMID:34308764
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8312598/
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.

摘要

上皮损伤和上皮内肥大细胞 (MC) 的增加是哮喘的特征。MC 介质胰蛋白酶和蛋白酶激活受体-2 (PAR2) 在上皮愈合中的作用尚未完全研究清楚。与对照组相比，胰蛋白酶刺激支气管上皮细胞 (BEC) 可促进间隙闭合、迁移和细胞速度。与对照组相比，受刺激的 BEC 中迁移标志物 CD151 的表达更高。与对照组相比，增殖标志物 KI67 在胰蛋白酶刺激的 BEC 中上调。与用胰蛋白酶刺激的 BEC 相比，用 PAR2 拮抗剂 I-191 处理可减少间隙闭合、迁移和细胞速度。我们发现胰蛋白酶通过增加迁移和增殖来增强上皮伤口愈合，这部分是通过 PAR2 调节的。我们的数据表明，在基线条件下组织修复时，胰蛋白酶可能是有益的。然而，在哮喘等病理情况下，由于激活的 MC 数量增加，它可能导致上皮重塑和功能丧失。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b0b/8312598/7570822b788f/KCAM_A_1950594_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b0b/8312598/d06c7edfb426/KCAM_A_1950594_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b0b/8312598/cdd4649e4e52/KCAM_A_1950594_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b0b/8312598/7388fe421832/KCAM_A_1950594_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b0b/8312598/49e1a047253f/KCAM_A_1950594_F0004_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b0b/8312598/7570822b788f/KCAM_A_1950594_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b0b/8312598/d06c7edfb426/KCAM_A_1950594_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b0b/8312598/cdd4649e4e52/KCAM_A_1950594_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b0b/8312598/7388fe421832/KCAM_A_1950594_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b0b/8312598/49e1a047253f/KCAM_A_1950594_F0004_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b0b/8312598/7570822b788f/KCAM_A_1950594_F0005_OC.jpg

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