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首页> 美国卫生研究院文献>Physiological Reports >Klf4 Klf2 and Zfp148 activate autophagy‐related genes in smooth muscle cells during aortic aneurysm formation
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Klf4 Klf2 and Zfp148 activate autophagy‐related genes in smooth muscle cells during aortic aneurysm formation

机译：Klf4Klf2和Zfp148在主动脉瘤形成过程中激活平滑肌细胞中的自噬相关基因

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摘要

Abdominal aortic aneurysms (AAAs) are a progressive dilation of the aorta that is characterized by an initial influx of inflammatory cells followed by a pro‐inflammatory, migratory, proliferative, and eventually apoptotic smooth muscle cell phenotype. In recent years, the mechanisms related to the initial influx of inflammatory cells have become well‐studied; the mechanisms related to chronic aneurysm formation, smooth muscle cell apoptosis and death are less well‐characterized. Autophagy is a generally believed to be a protective cellular mechanism that functions to recycle defective proteins and cellular organelles to maintain cellular homeostasis. Our goal with the present study was to investigate the role of autophagy in smooth muscle cells during AAA formation. Levels of the autophagy factors, Beclin, and LC3 were elevated in human and mouse AAA tissue via both qPCR and immunohistochemical analysis. Confocal staining in human and mouse AAA tissue demonstrated Beclin and LC3 were present in smooth muscle cells during AAA formation. Treatment of smooth muscle cells with porcine pancreatic elastase or interleukin (IL)‐1β activated autophagy‐related genes in vitro while treatment with a siRNA to Kruppel‐like transcription factor 4 (Klf4), Kruppel‐like transcription factor 2 (Klf2) or Zinc‐finger protein 148 (Zfp148) separately inhibited activation of autophagy genes. Chromatin immunoprecipitation assays demonstrated that Klf4, Klf2, and Zfp148 separately bind autophagy genes in smooth muscle cells following elastase treatment. These results demonstrate that autophagy is an important mechanism related to Klfs in smooth muscle cells during AAA formation.
机译：腹主动脉瘤（AAAs）是主动脉的渐进性扩张，其特征是炎症细胞开始大量涌入，随后是促炎性，迁移性，增殖性和最终凋亡的平滑肌细胞表型。近年来，与炎症细胞初始流入有关的机制已被充分研究。慢性动脉瘤形成，平滑肌细胞凋亡和死亡的相关机制尚不十分清楚。自噬通常被认为是一种保护性细胞机制，其功能是回收有缺陷的蛋白质和细胞器以维持细胞稳态。我们本研究的目标是研究AAA形成过程中自噬在平滑肌细胞中的作用。通过qPCR和免疫组织化学分析，人和小鼠AAA组织中自噬因子Beclin和LC3的水平均升高。在人和小鼠AAA组织中的共聚焦染色表明Beclin和LC3在AAA形成过程中存在于平滑肌细胞中。用猪胰弹性蛋白酶或白介素（IL）-1β激活的自噬相关基因体外处理平滑肌细胞，同时用siRNA处理Kruppel样转录因子4（Klf4），Kruppel样转录因子2（Klf2）或锌手指蛋白148（Zfp148）分别抑制自噬基因的激活。染色质免疫沉淀试验表明，弹性蛋白酶处理后，Klf4，Klf2和Zfp148分别结合自噬基因在平滑肌细胞中。这些结果表明自噬是与AAA形成过程中平滑肌细胞中Klfs有关的重要机制。

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