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Mast cell tryptase enhances wound healing by promoting migration in human bronchial epithelial cells
Cell Adhesion & Migration ( IF 3.2 ) Pub Date : 2021-07-24 , DOI: 10.1080/19336918.2021.1950594
Sofia Mogren 1 , Frida Berlin 1 , Sangeetha Ramu 1 , Asger Sverrild 2 , Celeste Porsbjerg 2 , Lena Uller 1 , Cecilia K Andersson 1
Affiliation  

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.



中文翻译:

肥大细胞类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

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 介质类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。与对照相比,用类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。与对照相比,受刺激的 BEC 具有更高的迁移标记 CD151 表达。与对照相比,增殖标记 KI67 在类胰蛋白酶刺激的 BEC 中上调。与用类胰蛋白酶刺激的 BEC 相比,用 PAR2 拮抗剂 I-191 处理可降低间隙闭合、迁移和细胞速度。我们发现类胰蛋白酶通过增加迁移和增殖来增强上皮伤口愈合,这部分通过 PAR2 进行调节。我们的数据表明类胰蛋白酶可能有益于基线条件下的组织修复。然而,在哮喘等病理情况下,激活的 MCs 数量增加,可能会导致上皮重塑和功能丧失。

更新日期:2021-07-25
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