ArticleJournal of stem cell research & therapy2014
Alcohol Disrupts Human Liver Stem/Progenitor Cell Proliferation and Differentiation.
Article in Journal of stem cell research & therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 17 citations in OpenAlex.
- Analysis of the factors influencing liver regeneration after hepatectomy in hepatocellular carcinoma patients and the relationship between liver regeneration and prognosis.Scientific reports · 2025Article
- Reduction of Cell Proliferation by Acute CCancers · 2021Article
- Liver regeneration and alcoholic liver disease.Annals of translational medicine · 2020Review
- Stem cells under the influence of alcohol: effects of ethanol consumption on stem/progenitor cells.Cellular and molecular life sciences : CMLS · 2019Review
- Sonic Hedgehog Signaling Regulates Hematopoietic Stem/Progenitor Cell Activation during the Granulopoietic Response to Systemic Bacterial Infection.Frontiers in immunology · 2018Article
- Impairment of Hematopoietic Precursor Cell Activation during the Granulopoietic Response to Bacteremia in Mice with Chronic-Plus-Binge Alcohol Administration.Infection and immunity · 2017Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
objectiveExcessive alcohol consumption injures the liver resulting in various liver diseases including liver cirrhosis. Advanced liver disease continues to be a major challenge to human health. Liver stem/progenitor cells (LSPCs) are tissue specific precursors with a distinct capacity of multi-lineage differentiation. These precursor cells may play an important role in the process of tissue injury repair and pathological transition of liver structures. At the present time, knowledge about the effect of alcohol on LSPC function during the development of alcoholic liver disease remains absent. This study was conducted to investigate changes in LSPC activity of proliferation and differentiation following alcohol exposure. The disruption of cell signaling mechanisms underlying alcohol-induced alteration of LSPC activities was also examined.
methodsPrimary and immortalized human liver stem cells (HL1-1 cells and HL1-hT1 cells, respectively) were cultured in media optimized for cell proliferation and hepatocyte differentiation in the absence and presence of ethanol. Changes in cell morphology, proliferation and differentiation were determined. Functional disruption of cell signaling components following alcohol exposure was examined.
resultsEthanol exposure suppressed HL1-1 cell growth [as measured by cell 5-bromo-2-deoxyuridine (BrdU) incorporation] mediated by epidermal growth factor (EGF) or EGF plus interleukin-6 (IL-6) in an ethanol dose-dependent manner. Similarly, ethanol inhibited BrdU incorporation into HL1-hT1 cells. Cyclin D1 mRNA expression by HL1-hT1 cells was suppressed when cells were cultured with 50 and 100 mM ethanol. Ethanol exposure induced morphological change of HL1-1 cells toward a myofibroblast-like phenotype. Furthermore, ethanol down-regulated E-cadherin expression while increasing collagen I expression by HL1-1 cells. Ethanol also stimulated Snail transcriptional repressor (Snail) and α-smooth muscle actin (α-SMA) gene expression by HL1-1 cells.
conclusionThese results demonstrate that the direct effect of alcohol on LSPCs is inhibiting their proliferation and promoting mesenchymal transition during their differentiation. Alcohol interrupts LSPC differentiation through interfering Snail signaling.
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Registered trials
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