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在人肺纤维细胞中,Endoplasmic网膜的压力诱导的衰老

Maunick Lefin Koloko Ngassie^1,2,3, Li Y Drake³, Benjamin B Roos³

¹Department of Pathology and Medical Biology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.

American journal of physiology. Lung cellular and molecular physiology

|May 21, 2024

概括

细胞内膜网膜 (ER) 应激驱动衰老的肺纤维细胞中的细胞衰老,有助于肺重塑. 这项研究将ER压力与衰老联系在一起,影响衰老肺部细胞外基质的产生.

科学领域:

细胞生物学细胞生物学
衰老研究研究衰老研究
肺部病理学肺部病理学

背景情况:

蛋白质稳定和细胞衰老的丧失是衰老的标志.
肺衰老中ER压力和细胞衰老之间的相互作用尚未研究.
老化肺部经历重塑,可能与这些细胞过程有关.

研究的目的:

描述ER应激反应和细胞衰老在人类肺纤维细胞跨年龄组.
研究ER压力,衰老和细胞外基质 (ECM) 生产之间的相互作用.
确定ER应激在与年龄相关的肺纤维细胞改变中的作用.

主要方法:

从年轻人和老年人身上培养出人类肺纤维细胞.
细胞被用载体,ER压力诱导剂 (MG132,埃托) 或ER压力抑制剂 (salubrinal) 治疗.
分析包括ER压力标志物 (ATF6,PERK),衰老标志物 (p21,SA-β-Gal),ECM标志物 (COL1A1,LUM) 和细胞因子水平 (IL-6,IL-8).

主要成果:

衰老的纤维细胞表现出更高的基线ER压力,衰老和ECM生产.
引发ER压力增加了衰老标志物和ECM的产生.
萨卢布林部分逆转了ER压力诱导的衰老,并抑制了ECM的产生.

结论:

在肺纤维细胞中建立和维持衰老方面,ER应激反应至关重要.
这种ER压力驱动的衰老有助于改变老化肺部的ECM重塑.
慢性ER压力在肺纤维细胞衰老和重塑中起着重要作用.

关键词:

衰老的衰老衰老的衰老细胞外矩阵是细胞外矩阵.蛋白质稳定性的丧失.肺肺肺肺肺肺肺肺肺改造改造改造改造改造改造

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