CLDN1沉默通过调节MMP14抑制气道平滑肌细胞的增殖和迁移。

IF 3.3 4区 医学 Q3 IMMUNOLOGY
Autoimmunity Pub Date : 2023-12-01 Epub Date: 2023-11-15 DOI:10.1080/08916934.2023.2281223
Wei Li, Linyan Liu, Ming'ai Duanqing, Xiaoqing Xiong, Dejian Gan, Jin Yang, Mingya Wang, Min Zhou, Jun Yan
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引用次数: 0

摘要

气道重塑是哮喘发展的重要病理因素。气道平滑肌细胞(ASMCs)的异常增殖和迁移是严重哮喘的重要病理机制。在目前的研究中,CLDN1被确定为哮喘相关基因,并在血小板衍生生长因子BB (PDGF-BB)刺激的ASMCs中上调。采用细胞计数试剂盒-8和EdU检测细胞增殖情况,transwell检测细胞迁移和侵袭情况。采用酶联免疫吸附法检测炎症因子水平。结果表明,CLDN1敲低抑制PDGF-BB治疗ASMCs的增殖、迁移、侵袭和炎症,而CLDN1过表达则表现出相反的作用。蛋白-蛋白相互作用和共免疫沉淀法显示CLDN1与基质金属蛋白酶14 (MMP14)直接相互作用。CLDN1正调控MMP14在哮喘中的表达,MMP14过表达逆转沉默CLDN1诱导的细胞增殖、迁移、侵袭和炎症。综上所述,CLDN1通过上调MMP14的表达,促进pdgf - bb诱导的ASMCs细胞增殖、迁移、侵袭和炎症反应,提示CLDN1在哮喘气道重塑中的潜在作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
CLDN1 silencing suppresses the proliferation and migration of airway smooth muscle cells by modulating MMP14.

Airway remodeling is an important pathologic factor in the progression of asthma. Abnormal proliferation and migration of airway smooth muscle cells (ASMCs) are important pathologic mechanisms in severe asthma. In the current study, claudin-1 (CLDN1) was identified as an asthma-related gene and was upregulated in ASMCs stimulated with platelet-derived growth factor BB (PDGF-BB). Cell counting kit-8 and EdU assays were used to evaluate cell proliferation, and transwell assay was carried out to analyze cell migration and invasion. The levels of inflammatory factors were detected using enzyme-linked immunosorbent assay. The results showed that CLDN1 knockdown inhibited the proliferation, migration, invasion, and inflammation of ASMCs treated with PDGF-BB, whereas overexpression of CLDN1 exhibited the opposite effects. Protein-protein interaction assay and co-immunoprecipitation revealed that CLDN1 directly interacted with matrix metalloproteinase 14 (MMP14). CLDN1 positively regulated MMP14 expression in asthma, and MMP14 overexpression reversed cell proliferation, migration, invasion, and inflammation induced by silenced CLDN1. Taken together, CLDN1 promotes PDGF-BB-induced cell proliferation, migration, invasion, and inflammatory responses of ASMCs by upregulating MMP14 expression, suggesting a potential role for CLDN1 in airway remodeling in asthma.

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来源期刊
Autoimmunity
Autoimmunity 医学-免疫学
CiteScore
5.70
自引率
8.60%
发文量
59
审稿时长
6-12 weeks
期刊介绍: Autoimmunity is an international, peer reviewed journal that publishes articles on cell and molecular immunology, immunogenetics, molecular biology and autoimmunity. Current understanding of immunity and autoimmunity is being furthered by the progress in new molecular sciences that has recently been little short of spectacular. In addition to the basic elements and mechanisms of the immune system, Autoimmunity is interested in the cellular and molecular processes associated with systemic lupus erythematosus, rheumatoid arthritis, Sjogren syndrome, type I diabetes, multiple sclerosis and other systemic and organ-specific autoimmune disorders. The journal reflects the immunology areas where scientific progress is most rapid. It is a valuable tool to basic and translational researchers in cell biology, genetics and molecular biology of immunity and autoimmunity.
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