GSE109140
Valproic acid attenuates hyperglycemia induced complement and coagulation cascade gene expression
Diabetes is a multifactorial disorder and epigenetics changes are increasingly appreciated to influence the development of diabetic complications. Chromatin remodeling and histone acetylation are implicated in activation of the inflammatory response. Recently, histone deacetylase (HDAC) inhibitors (HDACi) have proved to reduce the severity of inflammatory diseases. We have previously shown that chromatin alterations regulated by HDACi in HepG2 cells stimulated by hyperglycemia reduced hepatic glucose production. In this study, we examined gene expression patterns using next generation sequencing. We show the pharmacological HDAC inhibitor VPA attenuates hyperglycemia induced gene expression, highlighting the relevance of complement and coagulation cascade. These findings reveal a novel mechanism of VPA protection against hyperglycemia induced hepatic gene expression changes, which might improve the therapeutic approaches for diabetes. Overall design: RNA-seq was performed to understand gene expression changes in HepG2 cells in response to hyperglycemia and valproic acid. Analyses were performed in triplicate.