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Updated: Aug 9, 2026

Development of an Ethanol-induced Fibrotic Liver Model in Zebrafish to Study Progenitor Cell-mediated Hepatocyte Regeneration
Published on: May 13, 2016
Ethanol abrogates angiotensin II-stimulated vascular smooth muscle cell growth
Monique L Cain1, Robert L Hester, Ernest B Izevbigie
1Molecular Genetics and Molecular and Cellular Signaling Laboratory, Department of Biology, and National Institutes of Health Center for Environmental Health, Jackson State University, Jackson, MS 39217, USA.
Background:
Aberrant vascular smooth muscle cell (VSMC) proliferation is one of the etiological factors for hypertension and stroke. Angiotensin II (Ang II) and ethanol (EtOH) have been shown to modulate the proliferation of vascular smooth muscle cells (VSMCs) individually, but the combined effects of Ang II and EtOH on VSMC proliferative activities are unknown. The objective of this study was to determine the effects of EtOH, Ang II, and the combination of Ang II and EtOH on DNA synthesis, cell number, cyclic AMP (cAMP) production, and Mitogen-Activated Protein Kinase (MAPK) or (p44/42) activities in murine primary VSMCs.
Material And Methods:
Cell growth was determined by [3H] thymidine incorporation and confirmed by cell counts using a hemacytometer. Cyclic AMP assays were carried out using commercially available kits. MAPK activity was determined by immunoprecipitation studies using an ELK-1 fusion protein as a substrate.
Results:
Ang II (10 microM) stimulated DNA synthesis by four-fold (P < 0.05), cAMP production by 50% (P < 0.05), and MAPK (p44/42) activities by more than seven-fold (P < 0.01). In contrast, EtOH (100 mM) had no significant effects on DNA synthesis, cell number, and cAMP production. Ethanol exacerbated cAMP production by several fold but inhibited MAPK activity and subsequent cell growth induced by Ang II.
Conclusions:
These results suggest that EtOH elicits a regulatory effect on the Ang II signaling pathway.
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