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长非编码RNA GAS5通过通过miR-29c/HMGB1轴调节NF-κB,促进了Mycoplasma pneumoniae肺炎的发生

Juhua Ji^1,2, Fei Hong², Yi Liu³

¹Department of Respiratory Diseases, Children's Hospital of Soochow University.

The Tohoku journal of experimental medicine

|July 17, 2024

概括

GAS5通过降低 miR-29c 的调节来提高儿科 Mycoplasma pneumoniae 肺炎 (MPP) 的炎症,这通常会抑制 HMGB1. 沉默GAS5可以减少MPP的肺损伤和炎症.

科学领域:

分子生物学分子生物学
免疫学免疫学免疫学
儿科呼吸系统医学儿科呼吸系统医学

背景情况:

菌性肺炎肺炎 (MPP) 是一个重要的儿科健康问题.
之前在MPP患者中观察到高GAS5水平.
在MP引起的肺炎中GAS5的调节机制尚不清楚.

研究的目的:

阐明GAS5在Mycoplasma pneumoniae感染期间调节肺炎中的作用.
研究涉及MPP中的GAS5,miR-29c和HMGB1的分子途径.

主要方法:

通过鼻内MP注射构建一个MPP小鼠模型.
在实验室中用LAMPs刺激小鼠膜巨细胞 (AMs).
基因操纵 (敲击/过度表达) 和分子相互作用分析 (RNA-IP, luciferase 记者测定).

主要成果:

来自MPP小鼠的AM中,GAS5被上调,与HMGB1mRNA正相关.
miR-29c在MPP小鼠的AM中下调,与HMGB1.1负相关.
GAS5直接与miR-29c结合,miR-29c向HMGB1mRNA,抑制细胞灭绝,IL-6,TNF-α分泌和NF-κB激活.
过度表达GAS5逆转了miR-29c模仿效应;miR-29c抑制逆转了HMGB1的淘汰效应.
在MPP小鼠模型中,GAS5沉默改善了肺炎和损伤.

结论:

GAS5/miR-29c/HMGB1轴在MPP的发病过程中起着至关重要的作用.
这条通路通过NF-κB信号通路调节炎症和肺部组织病理损伤.

关键词:

气体5 气体5 是一个气体.这就是HMGB1的特点.菌性肺炎 (Mycoplasma pneumoniae) 是一种肺炎.通过NF-κB信号通路传递信号.在 miR-29c 中.

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