Alcohol Attenuated the Epithelial Phenotype in Liver HepG2 Cells Co-Cultured with K562 Cells
International Journal of Medical Toxicology and Forensic Medicine,
Vol. 16 (2026),
1 January 2026
,
Page 1-8
https://doi.org/10.22037/ijmtfm.v16.47083
Abstract
Background: Excessive drinking can cause liver damage and even liver fibrosis and cirrhosis. This study aimed to investigate the influence of alcohol and its related mechanisms on the transformation of growth factor-β1 (TGF-β1) and the loss of epithelial phenotype in hepatocytes.
Methods: In the present study, HepG2 cells (2 × 105 cells/ml) were co-cultured with K562 cells (2 × 105 cells/ml) and treated with 50 mM, 100 mM, and 200 mM alcohol for 24 hours. Cell morphology, as well as the expression of endothelial markers E-cadherin, Desmoplakin, CK18, and TGF-β1, were detected.
Results: The study showed that alcohol induced the loss of epithelial phenotype, considerably decreasing the mRNA levels of E-cadherin, Desmoplakin, and CK18, as well as E-cadherin protein expression. In contrast, alcohol increased the mRNA levels and concentrations of TGF-β1 in the cultured media of co-cultured HepG2 cells in a concentration-dependent manner. These results demonstrated that alcohol attenuated the epithelial phenotype in HepG2 cells co-cultured with K562 cells; meanwhile, K562 cells played an essential role in enhancing the expression of TGF-β1 in HepG2 cells.
Conclusion: Our research has established an in vitro model of alcohol-induced epithelial phenotype loss in hepatocytes and partly explained the mechanisms of alcohol-induced liver fibrosis.
- Alcohol, HepG2 cells, Co-cultured, TGF-β1, Epithelial phenotype loss
How to Cite
References
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