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. 2020 Sep 23;10:15558. doi: 10.1038/s41598-020-72172-7

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© The Author(s) 2020

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Expression of endothelin system genes increases in mouse experimental model and human AH. (a) Hepatic endothelin system gene expression was confirmed by qPCR from WT and Lcn2^−/− mice exposed to CCl₄ (n = 4–6). (b) Hepatic endothelin system gene expression from WT and Lcn2^−/− mice after 8-week ethanol plus binge exposure. (n = 4 for each group). (c) Human liver biopsies for RNA-sequencing analysis of EDN1, ECE1 and EDNRA expression included multiple etiologies of liver tissues representing control liver (n = 10), NASH (n = 9), HCV (n = 10), compensated cirrhosis (n = 9) and AH (n = 29). (d) Correlation of hepatic LCN2 and EDN1, ECE1 and EDNRA expression in AH patients. (e) Circulating ET1 concentration was quantified by ELISA in serum of patients with multiple etiologies of liver disease. *p < 0.05; **p < 0.01 by one-way ANOVA.