Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Aldehyde dehydrogenase 2 deficiency impairs cell proliferation in alcohol-fed mice

ABSTRACT: Serum samples from healthy male subjects with active ALDH2*1/*1 (G/G) or healthy male subjects with inactive ALDH2*1*/*2 (G/A) (n=5 per group) recruited from the First Affiliated Hospital of Jilin University (Changchun, China) for measurement of proteomic analysis post one-time acute alcohol drinking (0.4 g/kg).

ORGANISM(S): Mus Musculus

SUBMITTER: Yanhang Gao

PROVIDER: PXD065926 | iProX | Tue Jul 08 00:00:00 BST 2025

REPOSITORIES: iProX

ACCESS DATA

Json Xml

Publications

Aldehyde Dehydrogenase 2 Deficiency Impairs Liver Progenitor Cell Proliferation in Alcohol-Fed Mice.

Xiao Peng P Yang Siting S Bi Shenghua S Hao Yawen Y Zhang Feiyu F Ru Lin L Liu Tao T Qian Shengying S Zai Qiuhong Q Ma Ningning N Niu Junqi J He Yong Y Gao Yanhang Y

The American journal of pathology 20250903 1

Aldehyde dehydrogenase 2 (ALDH2) is a critical enzyme involved in the detoxification of acetaldehyde. Although numerous studies have demonstrated the significance of ALDH2 in alcohol-associated liver disease, its role in alcohol-induced activation of liver progenitor cells (LPCs) has not been thoroughly investigated. Proteomic analysis of serum samples from patients with either normal ALDH2 genotype or ALDH2 mutation following alcohol consumption revealed that ALDH2 deficiency may suppress LPC p ...[more]

PMID: 40912649

Similar Datasets

Characterization of ALDH2-deficient alcohol-associated liver disease (duodenum RNA seq)

Project description:Aldehyde dehydrogenase 2 (ALDH2) is a key enzyme to detoxify the ethanol first metabolite acetaldehyde. Approximately 8% world population have inactive ALDH2 and have facial flushing due to high levels of acetaldehyde after alcohol consumption. Alcohol-associated liver disease (ALD) and hepatocellular carcinoma (HCC) in those with inactive ALDH2 have not been characterized. ALD pathogeneses in these individuals are likely very different from those with normal ALDH2, different diagnosis criteria and treatment are required for these two populations. Here we studied ALD in inactive Aldh2 knockin (Aldh2KI) mice with chronic ethanol feeding.

2025-07-16 | GSE288043 | GEO

Peripheral blood gene-expression in heavy vs. moderate drinkers exposed to three types of personalized imagery

Project description:Alterations in stress-related gene-expression may play a role in stress-related drinking and the risk for alcohol dependence. Microarrays were used to measure changes in gene-expression in peripheral blood in non-smoking, social drinking subjects exposed to three types of personalized imagery: neutral, stressful (but not alcohol- related), and alcohol-related cues. Gene-expression was measured at baseline, immediately after, and 1 hour after stimulus presentation. Subjects were allowed to drink up to 750cc of beer in a “taste-test” following stimulus presentation in each imagery condition, and the amount of beer consumed was recorded. Gene-expression levels were compared in 2 groups of non-smoking subjects (n=11/group): heavy drinkers (HD, defined as regular alcohol use over the past year of at least 8 standard drinks/week for women and at least 15 standard drinks/week for men), and moderate drinkers (MD, defined as up to 7 standard drinks/week for women and 14 standard drinks/week for men).

2014-07-09 | GSE59206 | GEO

Chronic alcohol drinking compromises lung immunity by altering immunometabolism in both human and mouse lungs

Project description:Heavy alcohol drinking dysregulates lung immunity and host defense, which makes individuals with AUD more susceptible to develop inflammatory condition in lungs with poor prognosis. Current study, we focused on exploring the effects of chronic alcohol consumption on lungs using NIAAA alcohol feeding model in mice with 10 days of a Lieber-DeCarli liquid diet containing 5% ethanol followed by a single ethanol binge (5 g/kg) and population based human lung transcriptome data from Genotype-Tissue Expression (GTEx) project consist of 328 alcohol drinkers and 110 non-drinkers. Flow cytometry and transcriptomics analysis in mice lungs revealed that alcohol consumption dysregulates cellularity of immune cell levels and lung immunity. Transcriptomics analysis both in lungs and liver at 9-, 24- hours and 14 days post ethanol binge in mice uncovered that the lungs were more sensitive to alcohol effect to down-regulate pathways of immune system regulations than liver. Comparative data analysis of lung transcriptomes between mice and human subjects not only confirmed similar dysregulation on lung immunity but also provided evidence that immunometabolic changes are the central driver of alterations in lung transcriptome with down regulating immune pathways and upregulating metabolic pathways. Since the NIAAA model recapitulates multiple changes in the lung transcriptome that had been observed in human subjects with chronic alcohol drinking, this makes the mouse model suitable for experimental studies exploring role of alcohol drinking in lung health. Chronic alcohol drinking reduced mTOR signaling and cellularity of immune cells, which can be further attenuated by selective inhibition of mTOR. BCAA-mTOR signaling axis can be an upstream regulator of alcohol induced dysregulation in lung immunity

2024-07-22 | GSE248233 | GEO

microRNA Expression based, Effects of Chronic Intermittent Ethanol paradigm on mouse brain

Project description:We analyzed cerebral cortices (CTX) and midbrains (MB) from male C57BL/6J mice subjected to a CIE, 2BC paradigm, which induces heavy drinking and represents one of the best available animal models for alcohol dependence and relapse drinking.

2013-12-31 | GSE48576 | GEO

p53 regulates ethanol metabolism via ALDH2 modulating the development of alcoholic fatty liver disease

Project description:The tumor suppressor p53 is critical for tumor suppression and other biological events. Yet, the regulatory role of p53 in alcohol-induced fatty liver remains unclear. Here, we show a role for p53 in regulating the ethanol metabolism via acetaldehyde dehydrogenase 2 (ALDH2), a key enzyme responsible for oxidization of alcohol. Through repressing ethanol oxidization, p53 suppresses intracellular levels of acetyl-CoA and histone acetylation, leading to the inhibition of the stearoyl-CoA desaturase-1 (SCD1) gene expression. Mechanistically, p53 directly binds to ALDH2 and prevents the formation of its active tetramer, and indirectly limits the production of pyruvate that promotes the activity of ALDH2. Notably, p53 deficient mice exhibit increased lipid accumulation, which can be reversed by ALDH2 depletion. Moreover, hepatic specific knockdown of SCD1 diminishes ethanol-induced fatty liver caused by p53 loss. By contrast, overexpression of SCD1 in liver promotes ethanol-induced fatty liver development in wildtype mice, while has mild effect on p53-/- or ALDH2-/- mice. Overall, our findings reveal a previously unrecognized function of p53 in alcohol-induced fatty liver, and uncover pyruvate as a natural regulator of ALDH2.

2023-02-08 | GSE222743 | GEO

Empagliflozin Ameliorates Aldehyde Dehydrogenase 2 Deficiency-induced Endothelial Dysfunction

Project description:We conducted RNA sequcing of the homozygous and heterozygous of ALDH2*2 by using human induced pluripotent stem cell-derived endothelial cells (hiPSC-ECs)

2023-03-30 | GSE184419 | GEO

Peripheral blood gene-expression in heavy vs. moderate drinkers exposed to three types of personalized imagery

2014-07-09 | E-GEOD-59206 | biostudies-arrayexpress

Comparison of Differences in Gene Expression in the Nucleus Accumbens Shell of 5 Pairs of Rat Lines Selectively Bred for High or Low Alcohol Consumption

Project description:The objective of this study was to determine common innate differences in gene expression in the nucleus accumbens shell among the selectively bred (a) alcohol-preferring (P) vs. alcohol-non-preferring (NP) rats: (b) high-alcohol-drinking (HAD) vs. low-alcohol-drinking (LAD) rats (both replicates); (c) ALKO alcohol (AA) vs. nonalcohol (ANA) rats; and (d) Sardinian alcohol-preferring (sP) vs. alcohol-nonpreferring (sNP) rats.

2012-08-01 | GSE31705 | GEO

Comparison of Differences in Gene Expression in the Central Nucleus of the Amygdala (CeA) of 5 Pairs of Rat Lines Selectively Bred for High or Low Alcohol Consumption

Project description:The objective of this study was to determine common innate differences in gene expression in the Central Nucleus of the Amygdala (CeA) among the selectively bred (a) alcohol-preferring (P) vs. alcohol-non-preferring (NP) rats: (b) high-alcohol-drinking (HAD) vs. low-alcohol-drinking (LAD) rats (both replicates); (c) ALKO alcohol (AA) vs. nonalcohol (ANA) rats; and (d) Sardinian alcohol-preferring (sP) vs. alcohol-nonpreferring (sNP) rats.

2012-08-01 | GSE31708 | GEO

The effect of simulated night shift work on the circadian regulation of the human transcriptome

Project description:Eight healthy human subjects were enrolled in a 6-day simulated shift work protocol. Blood samples were collected during the two 24-hour measurement periods. Blood samples were collected every 4 hours during both measurement periods. Subjects entered the lab on Day 1. At the start of Day 2, the first 24-hour measurement period was started. Subjects slept according to their habitual sleep/wake schedule, followed by a 16-hour constant posture procedure. On days 3-6, the sleep period was delayed by 10 hours. Following the third night on this schedule, subjects underwent another 24-hour measurement period. During both measurement periods, 7 blood samples were collected and PBMCs were isolated. mRNA was extracted, labelled, and hybridized to microarrays.

2018-05-08 | GSE107537 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data