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慢性肝病中僵硬诱导的ERG转录因子调节

Stiffness-induced modulation of ERG transcription factor in chronic liver disease.

作者信息

Selicean Sonia-Emilia, Felli Eric, Wang Cong, Nulan Yeldos, Lozano Juan José, Guixé-Muntet Sergi, Ștefănescu Horia, Bosch Jaime, Berzigotti Annalisa, Gracia-Sancho Jordi

机构信息

Department of Visceral Surgery and Medicine, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland.

Department for BioMedical Research, Visceral Surgery and Medicine, University of Bern, Bern, Switzerland.

出版信息

NPJ Gut Liver. 2024;1(1):7. doi: 10.1038/s44355-024-00007-7. Epub 2024 Oct 1.

DOI:10.1038/s44355-024-00007-7
PMID:39381160
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11459910/
Abstract

Chronic liver disease (CLD) is characterised by liver sinusoidal endothelial cells (LSECs) dysfunction. Mechanical forces and inflammation are among the leading factors. ETS-related gene (ERG) is an endothelial-specific transcription factor, involved in maintaining cell quiescence and homeostasis. Our study aimed to understand the expression and modulation of ERG in CLD. ERG expression was characterised and correlated to clinical data in human liver cirrhosis at different disease stages. ERG dynamics in response to stiffness and inflammation were investigated in primary healthy and cirrhotic rat LSEC and in human umbilical vein endothelial cells (HUVECs). ERG is markedly downregulated in cirrhosis independently of disease stage or aetiology and its expression is modulated by substrate stiffness in ECs. Inflammation downregulates ERG in cells on physiological stiffness, but not on high stiffness, suggesting a complementary role of inflammation and stiffness in suppressing ERG. This study outlines ERG as an LSEC inflammation and stiffness-responsive transcription factor in cirrhosis.

摘要

慢性肝病（CLD）的特征是肝窦内皮细胞（LSEC）功能障碍。机械力和炎症是主要因素。ETS相关基因（ERG）是一种内皮特异性转录因子，参与维持细胞静止和稳态。我们的研究旨在了解CLD中ERG的表达和调节。对不同疾病阶段的人类肝硬化中ERG的表达进行了表征，并将其与临床数据相关联。在原代健康和肝硬化大鼠LSEC以及人脐静脉内皮细胞（HUVEC）中研究了ERG对硬度和炎症的动态反应。在肝硬化中，ERG明显下调，与疾病阶段或病因无关，其表达受内皮细胞底物硬度的调节。炎症在生理硬度条件下下调细胞中的ERG，但在高硬度条件下则不然，这表明炎症和硬度在抑制ERG方面具有互补作用。本研究概述了ERG作为肝硬化中LSEC炎症和硬度反应性转录因子的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/317e/11459910/e56590771662/44355_2024_7_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/317e/11459910/5bb7899d83bb/44355_2024_7_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/317e/11459910/e6e07557a4dc/44355_2024_7_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/317e/11459910/e56590771662/44355_2024_7_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/317e/11459910/5bb7899d83bb/44355_2024_7_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/317e/11459910/d06a85cb9b88/44355_2024_7_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/317e/11459910/e6e07557a4dc/44355_2024_7_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/317e/11459910/e56590771662/44355_2024_7_Fig4_HTML.jpg

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本文引用的文献

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Mechanobiology of portal hypertension.门静脉高压症的力学生物学
JHEP Rep. 2023 Aug 2;5(11):100869. doi: 10.1016/j.jhepr.2023.100869. eCollection 2023 Nov.
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ERG通过Wnt3a/β-连环蛋白途径转录激活SFRP1，以促进瘢痕疙瘩成纤维细胞的凋亡，并抑制上皮-间质转化和纤维化。
Arch Dermatol Res. 2025 Feb 22;317(1):467. doi: 10.1007/s00403-025-03902-y.
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Dysfunctional ERG signaling drives pulmonary vascular aging and persistent fibrosis.功能失调的 ERG 信号驱动肺血管老化和持续纤维化。
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