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Expression profiling comparisons of human PBMC treated with class I/IIb or class IIa HDAC inhibitors

ABSTRACT: The aim of this study was to identify differential gene expression resulting from the inhibition of class IIa HDACs in human PBMC.

ORGANISM(S): Homo sapiens

PROVIDER: GSE44621 | GEO | 2013/03/24

SECONDARY ACCESSION(S): PRJNA190665

REPOSITORIES: GEO

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Expression profiling comparisons of human PBMC treated with class I/IIb or class IIa HDAC inhibitors

Project description:The aim of this study was to identify differential gene expression resulting from the inhibition of class IIa HDACs in human PBMC. Human PBMC were cultured ex vivo with a mitogenic stimulus (1 ug/ml phytohemagglutinin, PHA) for 60 hours concurrent with exposure to vehicle (DMSO), vorinostat (3 uM), or TMP195 (3 uM). In addition to the whole PBMC populations, a portion of the cultures treated with DMSO or TMP195 were used for FACS purification of mutually exclusive CD3+ (T cell), CD19+ (B cell), and CD14+ (monocyte) populations. All samples were then processed for RNA extraction, labeling, and hybridization to Affymetrix arrays. Vehicle vs. vorinostat vs. TMP195 treatments in PBMC; Vehicle vs. TMP195 treatment in CD3+, CD19+ or CD14+ cells

2013-03-24 | E-GEOD-44621 | biostudies-arrayexpress

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Project description:Analysis of Class II Histone Deacetylase (HDAC) regulation of hepatic gluconeogenesis at the gene expression level. We show that in liver, Class IIa HDACs (HDAC4, 5, and 7) are all phosphorylated and excluded from the nucleus by AMPK family kinases. In response to the fasting hormone glucagon, Class IIa HDACs rapidly translocate to the nucleus where they directly bind to the promoters of gluconeogenic enzymes such as G6Pase. In turn, HDAC4/5 mediate the acute transcriptional induction of these genes via deacetylation and activation of Foxo family transcription factors. Loss of Class IIa HDACs in the murine liver results in inhibition of FOXO target genes and lowers blood glucose, resulting in increased glycogen storage. Total RNA obtained from primary hepatocytes infected with shGFP or shHDAC4 & 5 subjected to 2 or 4 hours treatment with DMSO or forskolin.

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Project description:Histone deacetylases (HDACs) are long recognized for important functions in regulating gene transcription in biology and diseases. However, unlike for ubiquitously expressed class I HDACs, we have little mechanistic understanding of class II HDACs that have postulated tissue specific functions. Here we report that class IIa Hdac4 and Hdac7 are up-regulated in transcription through IL-6-Stat3 signaling selectively in mouse T-helper 17 (Th17) cells during lineage-specific differentiation, but not in Th1, Th2, and Treg subtypes. Genetic knockout of Hdac4 or Hdac7 established their importance for Th17 differentiation with different functional mechanisms. Hdac4 works with Th17 transcription factors JunB-Irf4-Batf for transcriptional activation of Th17 signature genes Il17a/f, whereas Hdac7 acts distinctively in concert with Aiolos/Ncor1/Hdac3 co-repressor complex for transcriptional repression of Th17 negative regulators including Il2. Pharmacological inhibition or gene knockout of Hdac4 and Hdac7 ameliorates development of T-cell transfer induced colitis and experimental autoimmune encephalomyelitis (EAE) in mice through blockage of Th17 cell development in colon and central nervous system that recapitulate inflammatory bowel diseases and multiple sclerosis in humans, respectively. Our study highlights a previously unknown distinct mechanisms of Hdac4 and Hdac7 in transcriptional control of Th17 cell development, and rationalizes a new therapeutic strategy of targeting class IIa HDAC4/7 for the treatment of Th17-related inflammatory and autoimmune diseases.

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