SREBP1c mediates the effect of acetaldehyde on Cidea expression in Alcoholic fatty liver Mice

Abstract Cell death inducing DNA fragmentation factor-alpha-like A (Cidea) is a member of cell death-inducing DFF45-like effector (CIDE) protein. The initial function of CIDE is the promotion of cell death and DNA fragmentation in mammalian cells. Cidea was recently reported to play critical roles i...

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Autores principales: Qi He, Yan Diao, Tingting Zhao, Baoyu Hou, Linel Darrel Ngokana, Huan Liang, Junhui Nie, Peizhu Tan, Hui Huang, Yanze Li, Lin Qi, Yuanyuan Zhao, Ying Liu, Xu Gao, Lingyun Zhou
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Publicado: Nature Portfolio 2018
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Acceso en línea:https://doaj.org/article/1285309531e3487a9bfe582702b1f496
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spelling oai:doaj.org-article:1285309531e3487a9bfe582702b1f4962021-12-02T15:08:58ZSREBP1c mediates the effect of acetaldehyde on Cidea expression in Alcoholic fatty liver Mice10.1038/s41598-018-19466-z2045-2322https://doaj.org/article/1285309531e3487a9bfe582702b1f4962018-01-01T00:00:00Zhttps://doi.org/10.1038/s41598-018-19466-zhttps://doaj.org/toc/2045-2322Abstract Cell death inducing DNA fragmentation factor-alpha-like A (Cidea) is a member of cell death-inducing DFF45-like effector (CIDE) protein. The initial function of CIDE is the promotion of cell death and DNA fragmentation in mammalian cells. Cidea was recently reported to play critical roles in the development of hepatic steatosis. The purpose of present study is to determine the effect of chronic alcohol intake on Cidea expression in the livers of mice with alcoholic fatty liver disease. Cidea expression was significantly increased in the liver of alcohol-induced fatty liver mice. While, knockdown of Cidea caused lipid droplets numbers reduction. Next, we detected the activity of ALDH2 reduction and the concentration of serum acetaldehyde accumulation in our alcohol-induced fatty liver mice. Cidea expression was elevated in AML12 cells exposed to 100uM acetaldehyde. Interestingly, Dual-luciferase reporter gene assay showed that 100 uM acetaldehyde led to the activation of Cidea reporter gene plasmid which containing SRE element. What’s more, the knockdown of SREBP1c suppressed acetaldehyde-induced Cidea expression. Overall, our findings suggest that Cidea is highly associated with alcoholic fatty liver disease and Cidea expression is specifically induced by acetaldehyde, and this up-regulation is most likely mediated by SREBP1c.Qi HeYan DiaoTingting ZhaoBaoyu HouLinel Darrel NgokanaHuan LiangJunhui NiePeizhu TanHui HuangYanze LiLin QiYuanyuan ZhaoYing LiuXu GaoLingyun ZhouNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 8, Iss 1, Pp 1-10 (2018)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Qi He
Yan Diao
Tingting Zhao
Baoyu Hou
Linel Darrel Ngokana
Huan Liang
Junhui Nie
Peizhu Tan
Hui Huang
Yanze Li
Lin Qi
Yuanyuan Zhao
Ying Liu
Xu Gao
Lingyun Zhou
SREBP1c mediates the effect of acetaldehyde on Cidea expression in Alcoholic fatty liver Mice
description Abstract Cell death inducing DNA fragmentation factor-alpha-like A (Cidea) is a member of cell death-inducing DFF45-like effector (CIDE) protein. The initial function of CIDE is the promotion of cell death and DNA fragmentation in mammalian cells. Cidea was recently reported to play critical roles in the development of hepatic steatosis. The purpose of present study is to determine the effect of chronic alcohol intake on Cidea expression in the livers of mice with alcoholic fatty liver disease. Cidea expression was significantly increased in the liver of alcohol-induced fatty liver mice. While, knockdown of Cidea caused lipid droplets numbers reduction. Next, we detected the activity of ALDH2 reduction and the concentration of serum acetaldehyde accumulation in our alcohol-induced fatty liver mice. Cidea expression was elevated in AML12 cells exposed to 100uM acetaldehyde. Interestingly, Dual-luciferase reporter gene assay showed that 100 uM acetaldehyde led to the activation of Cidea reporter gene plasmid which containing SRE element. What’s more, the knockdown of SREBP1c suppressed acetaldehyde-induced Cidea expression. Overall, our findings suggest that Cidea is highly associated with alcoholic fatty liver disease and Cidea expression is specifically induced by acetaldehyde, and this up-regulation is most likely mediated by SREBP1c.
format article
author Qi He
Yan Diao
Tingting Zhao
Baoyu Hou
Linel Darrel Ngokana
Huan Liang
Junhui Nie
Peizhu Tan
Hui Huang
Yanze Li
Lin Qi
Yuanyuan Zhao
Ying Liu
Xu Gao
Lingyun Zhou
author_facet Qi He
Yan Diao
Tingting Zhao
Baoyu Hou
Linel Darrel Ngokana
Huan Liang
Junhui Nie
Peizhu Tan
Hui Huang
Yanze Li
Lin Qi
Yuanyuan Zhao
Ying Liu
Xu Gao
Lingyun Zhou
author_sort Qi He
title SREBP1c mediates the effect of acetaldehyde on Cidea expression in Alcoholic fatty liver Mice
title_short SREBP1c mediates the effect of acetaldehyde on Cidea expression in Alcoholic fatty liver Mice
title_full SREBP1c mediates the effect of acetaldehyde on Cidea expression in Alcoholic fatty liver Mice
title_fullStr SREBP1c mediates the effect of acetaldehyde on Cidea expression in Alcoholic fatty liver Mice
title_full_unstemmed SREBP1c mediates the effect of acetaldehyde on Cidea expression in Alcoholic fatty liver Mice
title_sort srebp1c mediates the effect of acetaldehyde on cidea expression in alcoholic fatty liver mice
publisher Nature Portfolio
publishDate 2018
url https://doaj.org/article/1285309531e3487a9bfe582702b1f496
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