Pharmacological HDAC inhibition impairs pancreatic β-cell function through an epigenome-wide reprogramming.

ABSTRACT: Histone deacetylases enzymes (HDACs) are chromatin modifiers that regulate gene expression through deacetylation of lysine residues within specific histone and non-histone proteins. A cell-specific gene expression pattern defines the identity of insulin-producing pancreatic β cells, yet molecular networks driving this transcriptional specificity are not fully understood. Here, we investigated the HDAC-dependent molecular mechanisms controlling pancreatic β-cell identity and function using the pan-HDAC inhibitor trichostatin A through chromatin immunoprecipitation assays and RNA sequencing experiments. We observed that TSA alters insulin secretion associated with β-cell specific transcriptome programming in both mouse and human β-cell lines, as well as on human pancreatic islets. We also de

SUBMITTER: Oger F 

PROVIDER: S-EPMC10366467 | biostudies-literature | 2023 Jul

REPOSITORIES: biostudies-literature