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MiR-4454 in Combined Allergic Rhinitis and Asthma Syndrome (CARAS):Clinical significance and mechanistic insights into airway inflammation

哮喘 医学 气道 免疫学 炎症 临床意义 过敏性哮喘 内科学 麻醉
作者
Zhiguang Liu,Chuang Sun,Yujia Shi,Zhipeng Wang,Lianzheng Zhou,Qian Zhang,Zhengdao Mao
出处
期刊:Cellular and Molecular Biology [Cellular and Molecular Biology Association]
卷期号:70 (3): 225-232 被引量:3
标识
DOI:10.14715/cmb/2024.70.3.34
摘要

Abnormal expression of non-coding microRNA is associated with the development of combined allergic rhinitis and asthma syndrome (CARAS). However, the function of miR-4454 in CARAS is unknown. Our study aimed to reveal the clinical significance and related mechanism of miR-4454 in CARAS. Blood samples from 38 cases of CARAS and 43 cases of healthy subjects were collected to detect the expression of miR-4454. House dust mite (HDM) sensitization and challenge-induced bronchial epithelial cells to simulate the asthma state model in vitro, miR-4454 mimics and inhibitor transfection to detect the expression level of pro-inflammatory cytokines, cell survival rate and migration ability, flow cytometry and western blot (WB) Detection of cell cycle, apoptosis and inflammation-related protein levels. Compared with healthy controls, the expression of miR-4454 in the blood of CARAS patients was significantly up-regulated, and IL-6 and IL-8 were significantly up-regulated in the HDM treatment group, indicating that the model induction was successful. After overexpression of miR-4454, cell proliferation and migration in the HDM-treated group were significantly inhibited, and the levels of early apoptosis and inflammation-related proteins (IL-17, IL-17RD, TNF-α, GCSF and NF-κB) were increased High; after inhibiting miR-4454, cell proliferation and migration were significantly enhanced, and the levels of apoptosis and inflammation-related proteins were decreased. This study found that inhibiting the expression of miR-4454 can improve HDM-induced cell injury, which may be related to miR-4454 regulating the activation of IL-17/NF-кB inflammatory axis.
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