A549电池
脂多糖
小RNA
细胞凋亡
基因沉默
促炎细胞因子
MAPK/ERK通路
炎症
肿瘤坏死因子α
下调和上调
医学
癌症研究
药理学
免疫学
信号转导
细胞生物学
化学
生物
基因
生物化学
作者
Siliang Zhu,Wenke Song,Yanqi Sun,Yong-qin Zhou,Fanpo Kong
标识
DOI:10.1111/1440-1681.13315
摘要
Abstract Micro RNA (miRNA) and mitogen‐activated protein kinase (MAPK) are reported as the crucial regulators of inflammatory responses in acute lung injury (ALI). This study will explore the role of the miR‐342/MAPK1 axis in regulation of lipopolysaccharide (LPS)‐induced ALI. We found that miR‐342 was down‐regulated in LPS‐induced A549 cells compared with the control group with DMSO, accompanied by elevated inflammatory cytokines and apoptosis. Over‐expression of miR‐342 reduced LPS‐induced inflammatory responses and apoptosis in LPS‐stimulated A549 cells, and had a protective role in LPS‐treated mice with ALI by decreasing levels of inflammatory cytokines, improving survival of mice with ALI, and ameliorating the lung permeability. Dual‐luciferase reporter gene assay demonstrated that miR‐342 regulated the expression of MAPK1 by directly targeting its 3′ untranslated region (3′‐UTR). Mechanistically, MAPK1 silencing abrogated LPS‐induced inflammatory injury in A549 cells, and partially enhanced the protective effect of miR‐342. Therefore, miR‐342 attenuates LPS‐induced ALI by targeting MAPK1 expression, thereby protecting against A549 cell injury induced by LPS and lung injury of mice with ALI.
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