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

IF 4.3 3区材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC ACS Applied Electronic Materials Pub Date : 2021-12-01 DOI:10.1080/19336918.2021.1950594

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

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引用次数: 8

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.

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肥大细胞胰蛋白酶通过促进人支气管上皮细胞的迁移来促进伤口愈合。

上皮损伤和上皮内肥大细胞(MC)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)在上皮伤口愈合中的作用尚未得到充分研究。与对照组相比，胰蛋白酶刺激支气管上皮细胞(BECs)可促进间隙关闭、迁移和细胞速度。与对照组相比，受刺激的BECs具有更高的迁移标志物CD151的表达。与对照组相比，增殖标志物KI67在胰蛋白酶刺激的BECs中上调。与胰蛋白酶刺激的BECs相比，PAR2拮抗剂I-191治疗减少了间隙关闭、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促进上皮伤口愈合，这在一定程度上是由PAR2调节的。我们的数据表明，在基线条件下，胰蛋白酶可能对组织修复有益。然而，在病理学背景下，如哮喘中活化的MCs数量增加，它可能导致上皮重塑和功能丧失。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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