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通过S100A2的激活,通过FoxO1-介导的上皮细胞-介质细胞过渡促进脏的间歇性纤维化

Xuejia Yang¹, Fan Zheng¹, Penghua Yan²

¹Zhejiang Key Laboratory of Intelligent Cancer Biomarker Discovery and Translation, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325035, China.

Cell biology and toxicology

|October 9, 2024

概括

通过与FoxO1.1的相互作用,S100A2蛋白通过驱动上皮层-介质细胞过渡 (EMT) 来促进纤维化. 抑制S100A2或FoxO1可以降低慢性病中的纤维化和细胞外矩阵积累.

科学领域:

腎臟病學 (nephrology) 是一種醫學專業.
分子生物学分子生物学
细胞生物学细胞生物学

背景情况:

脏间歇性纤维化 (RIF) 是慢性脏疾病 (CKD) 的一个标志.
表皮-介质细胞过渡 (EMT) 是驱动RIF的一个关键机制.
在RIF病原体中S100A2的作用尚不清楚.

研究的目的:

调查S100A2在间位纤维化 (RIF) 中的作用和分子机制.
在EMT和RIF的背景下探索S100A2和FoxO1之间的关系.

主要方法:

在小鼠模型 (UUO,IRI,AAN) 和TGF-β1治疗的HK-2细胞中分析了S100A2表达.
功能增益和丧失研究 (siRNA,过度表达) 在体外进行.
这些技术包括RT-qPCR,免疫阻塞,免疫光和共免疫沉 (Co-IP).
使用了转录组测序和药理阻断.

主要成果:

在RIF模型和TGF-β1治疗细胞中,S100A2表达升高.
S100A2的过度表达诱导了EMT和细胞外基质 (ECM) 沉积,而S100A2的淘汰抑制了这些过程.
S100A2与FoxO1相互作用,影响其酸化和激活.
在S100A2沉默细胞中,FoxO1阻塞挽救了TGF-β1诱导的EMT和ECM沉积.

结论:

激活S100A2会加剧脏间歇性纤维化.
S100A2促进了FoxO1介导的EMT,为RIF做出了贡献.
准S100A2或FoxO1可能为CKD提供治疗策略.

关键词:

这是一个ECM,ECM是ECM.在EMT中,EMT是EMT.在FoxO1上,FoxO1是FoxO1的第一个代号.在RIF中,RIF是RIF.在 S100A2 中使用.

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