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Valproic acid influences the expression of genes implicated with hyperglycaemia-induced complement and coagulation
Marina Barreto Felisbino1,2, Mark Ziemann2, Ishant Khurana2
1Department of Structural and Functional Biology, Institute of Biology, University of Campinas (Unicamp), Campinas, SP, 13083-862, Brazil.
Scientific Reports
|January 26, 2021
Summary
Valproic acid (VPA) reverses hyperglycemia-induced changes in liver cells by modulating gene expression. This histone deacetylase inhibitor shows potential in attenuating inflammatory and coagulation pathways.
Area of Science:
- Hepatology
- Molecular Biology
- Pharmacology
Background:
- The liver is crucial for metabolic homeostasis and producing clotting/immune factors.
- Hyperglycemia induces significant changes in hepatocyte chromatin and metabolism.
- Previous work indicated valproic acid (VPA) can reverse some metabolic alterations.
Purpose of the Study:
- To investigate the impact of VPA on gene expression in hepatocytes under hyperglycemic conditions.
- To explore the mechanisms by which VPA influences hepatic cell activation.
Main Methods:
- RNA-sequencing (RNA-seq) was employed to analyze gene expression changes.
- Hepatocytes were studied under hyperglycemic conditions with and without VPA treatment.
Main Results:
- VPA was observed to attenuate the activation of complement and coagulation cascade genes induced by hyperglycemia.
- Gene activation events were correlated with alterations in histone acetylation at gene promoters.
- Epigenetic regulation by VPA was implicated in its observed effects.
Conclusions:
- VPA demonstrates a capacity to modulate gene expression in hepatocytes, specifically counteracting hyperglycemia-induced inflammatory and coagulation pathways.
- Epigenetic modifications, particularly histone acetylation, play a role in VPA's therapeutic action.
- VPA presents a potential pharmacological strategy for managing hyperglycemia-related hepatic dysfunction.
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