Paralemmin-3 通过缺口信号通路增强脂多糖诱导的急性肺损伤与 M1 巨噬细胞极化作用

IF 1.9 4区医学 Q3 PHYSIOLOGY

Respiratory Physiology & Neurobiology Pub Date : 2023-12-14 DOI:10.1016/j.resp.2023.104203

Xuxin Chen , Fan Wang , Jian Tang , Jiguang Meng, Zhihai Han

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引用次数: 0

摘要

背景急性肺损伤（ALI）包括严重的肺损伤和呼吸衰竭，并伴随着肺泡巨噬细胞（AM）的活化。方法通过连续吸入脂多糖（LPS）建立 ALI 大鼠模型。分析了 PALM3 对大鼠存活率、肺损伤严重程度和巨噬细胞极化的影响。结果PALM3过表达会增加ALI大鼠的死亡率，加重肺部病理损伤，并促进AM向M1细胞极化。相反，PALM3 基因敲除则会产生相反的效果。结论在LPS诱导的ALI中，PALM3通过激活Notch信号通路加重肺损伤并诱导巨噬细胞向M1细胞极化，这可能对ALI/ARDS的治疗有所启示。

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Paralemmin-3 augments lipopolysaccharide-induced acute lung injury with M1 macrophage polarization via the notch signaling pathway

Background

Acute lung injury (ALI) involves severe lung damage and respiratory failure, which are accompanied by alveolar macrophage (AM) activation. The aim of this article is to verify the influence of paralemmin-3 (PALM3) on alveolar macrophage (AM) polarization in ALI and the underlying mechanism of action.

Methods

An ALI rat model was established by successive lipopolysaccharide (LPS) inhalations. The influence of PALM3 on the survival rate, severity of lung injury, and macrophage polarization was analyzed. Furthermore, we explored the underlying mechanism of PALM3 in regulating macrophage polarization.

Results

PALM3 overexpression increased mortality of ALI rats, augmented lung pathological damage, and promoted AM polarization toward M1 cells. Conversely, PALM3 knockdown had the opposite effects. Mechanistically, PALM3 might promote M1 polarization by acting as an adaptor to facilitate transduction of Notch signaling.

Conclusion

PALM3 aggravates lung injury and induces macrophage polarization toward M1 cells by activating the Notch signaling pathway in LPS-induced ALI, which may shed light on ALI/ARDS treatments.

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来源期刊

Respiratory Physiology & Neurobiology 医学-呼吸系统

CiteScore

4.80

自引率

8.70%

发文量

104

审稿时长

54 days

期刊介绍： Respiratory Physiology & Neurobiology (RESPNB) publishes original articles and invited reviews concerning physiology and pathophysiology of respiration in its broadest sense. Although a special focus is on topics in neurobiology, high quality papers in respiratory molecular and cellular biology are also welcome, as are high-quality papers in traditional areas, such as: -Mechanics of breathing- Gas exchange and acid-base balance- Respiration at rest and exercise- Respiration in unusual conditions, like high or low pressure or changes of temperature, low ambient oxygen- Embryonic and adult respiration- Comparative respiratory physiology. Papers on clinical aspects, original methods, as well as theoretical papers are also considered as long as they foster the understanding of respiratory physiology and pathophysiology.