KLF13通过结合PGC-1α调节线粒体质量控制,减轻脂多糖诱导的肺泡上皮细胞损伤。

IF 1.9 4区 医学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Journal of Interferon and Cytokine Research Pub Date : 2024-07-01 DOI:10.1089/jir.2023.0234
Qiong Xi, Lin Liu, Qin Zhao, Shan Zhu
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引用次数: 0

摘要

败血症是一种危及生命的临床综合征,急性肺损伤是最早也是最严重的并发症。我们的目的是评估克虏伯样因子13(KLF13)在脂多糖(LPS)诱导的人肺泡II型上皮细胞损伤中的作用,并揭示与过氧化物酶体增殖体激活受体-γ共激活因子1-α(PGC-1α)相关的可能机制。在 LPS 处理的 A549 细胞中,无论是否过表达 KLF13 或敲除 PGC-1α,细胞存活率都是通过细胞计数试剂盒-8 法测定的。酶联免疫吸附测定试剂盒检测了炎症因子的水平,末端脱氧核苷酸转移酶 dUTP 缺口端标记染色检测了细胞凋亡。此外,线粒体活性氧(MitoSOX)和线粒体膜电位的检测采用了线粒体活性氧红染色法和JC-1染色法。线粒体质量控制(MQC)相关蛋白的表达通过 Western 印迹进行评估。共免疫沉淀(Co-IP)法分析了KLF13和PGC-1α之间的相互作用。结果表明,KLF13在LPS处理的A549细胞中高表达。KLF13 的上调提高了暴露于 LPS 的 A549 细胞的存活率并降低了炎症因子的水平。此外,KLF13的功能增益抑制了LPS诱导的A549细胞凋亡,同时上调了BCL2的表达,下调了Bax和裂解caspase3的表达。此外,KLF13 的过表达还能改善 MQC,表现为 MitoSOX、JC-1 单体减少,JC-1 聚集体增加,以及与 MQC 相关的蛋白质发生变化。此外,Co-IP分析证实了KLF13与PGC-1α之间的相互作用。PGC-1α的缺乏恢复了KLF13上调对LPS处理的A549细胞的炎症、凋亡和MQC的影响。总之,KLF13通过结合PGC-1α调节MQC,从而减轻了LPS诱导的肺泡上皮细胞炎症和凋亡。
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KLF13 Attenuates Lipopolysaccharide-Induced Alveolar Epithelial Cell Damage by Regulating Mitochondrial Quality Control via Binding PGC-1α.

Sepsis is a clinically life-threatening syndrome, and acute lung injury is the earliest and most serious complication. We aimed to assess the role of kruppel-like factor 13 (KLF13) in lipopolysaccharide (LPS)-induced human alveolar type II epithelial cell damage and to reveal the possible mechanism related to peroxisome proliferator-activated receptor-γ co-activator 1-α (PGC-1α). In LPS-treated A549 cells with or without KLF13 overexpression or PGC-1α knockdown, cell viability was measured by a cell counting kit-8 assay. Enzyme-linked immunosorbent assay kits detected the levels of inflammatory factors, and terminal deoxynucleotidyl transferase dUTP nick-end labeling staining measured cell apoptosis. Besides, mitochondrial reactive oxygen species (MitoSOX) and mitochondrial membrane potential were detected using MitoSOX red- and JC-1 staining. Expression of proteins related to mitochondrial quality control (MQC) was evaluated by western blot. Co-immunoprecipitation (Co-IP) assay was used to analyze the interaction between KLF13 and PGC-1α. Results indicated that KLF13 was highly expressed in LPS-treated A549 cells. KLF13 upregulation elevated the viability and reduced the levels of inflammatory factors in A549 cells exposed to LPS. Moreover, KLF13 gain-of-function inhibited LPS-induced apoptosis of A549 cells, accompanied by upregulated BCL2 expression and downregulated Bax and cleaved caspase3 expression. Furthermore, MQC was improved by KLF13 overexpression, as evidenced by decreased MitoSOX, JC-1 monomers and increased JC-1 aggregates, coupled with the changes of proteins related to MQC. In addition, Co-IP assay confirmed the interaction between KLF13 and PGC-1α. PGC-1α deficiency restored the impacts of KLF13 upregulation on the inflammation, apoptosis, and MQC in LPS-treated A549 cells. In conclusion, KLF13 attenuated LPS-induced alveolar epithelial cell inflammation and apoptosis by regulating MQC via binding PGC-1α.

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来源期刊
CiteScore
3.80
自引率
0.00%
发文量
78
审稿时长
2.2 months
期刊介绍: Journal of Interferon & Cytokine Research (JICR) provides the latest groundbreaking research on all aspects of IFNs and cytokines. The Journal delivers current findings on emerging topics in this niche community, including the role of IFNs in the therapy of diseases such as multiple sclerosis, the understanding of the third class of IFNs, and the identification and function of IFN-inducible genes.
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