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The critical roles of histone deacetylase 3 in the pathogenesis of solid organ injury.

ABSTRACT: Histone deacetylase 3 (HDAC3) plays a crucial role in chromatin remodeling, which, in turn, regulates gene transcription. Hence, HDAC3 has been implicated in various diseases, including ischemic injury, fibrosis, neurodegeneration, infections, and inflammatory conditions. In addition, HDAC3 plays vital roles under physiological conditions by regulating circadian rhythms, metabolism, and development. In this review, we summarize the current knowledge of the physiological functions of HDAC3 and its role in organ injury. We also discuss the therapeutic value of HDAC3 in various diseases.

SUBMITTER: Ning L

PROVIDER: S-EPMC8302660 | biostudies-literature | 2021 Jul

REPOSITORIES: biostudies-literature

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The critical roles of histone deacetylase 3 in the pathogenesis of solid organ injury.

Ning Li L Rui Xiong X Bo Wang W Qing Geng G

Cell death & disease 20210723 8

Histone deacetylase 3 (HDAC3) plays a crucial role in chromatin remodeling, which, in turn, regulates gene transcription. Hence, HDAC3 has been implicated in various diseases, including ischemic injury, fibrosis, neurodegeneration, infections, and inflammatory conditions. In addition, HDAC3 plays vital roles under physiological conditions by regulating circadian rhythms, metabolism, and development. In this review, we summarize the current knowledge of the physiological functions of HDAC3 and it ...[more]

PMID: 34301918

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Project description:Histone deacetylases (HDAC) are enzymes that modify key residues in histones to regulate chromatin architecture, and play a vital role in cell survival, cell cycle progression, and tumorigenesis. To understand the function of Hdac3, a critical component of the N-CoR/SMRT repression complex, a conditional allele of Hdac3 was engineered. Given the vital role of HDAC3 in normal cells and in the generation and treatment of various cancers, a conditional deletion of Hdac3 was engineered in mice. The deletion of Hdac3 in the germ line yielded very early embryonic lethality. Therefore, mouse embryonic-derived fibroblasts (MEFs) containing the Hdac3 conditional allele were used to examine the function of Hdac3 in cell viability and in cell cycle control. Given the links between Hdac3 and transcriptional repression, we used oligonucleotide micro arrays to examine RNA isolated from control and Cre recombinase expressing MEFs to define the changes in gene expression upon inactivation of Hdac3. Initially, we compared RNA from Ad-Cre infected Hdac3FL/+ and Hdac3FL/- MEFs and then we extended the analysis to Hdac3FL/- MEFs expressing Cre-ER (tamoxifen responsive Cre-estrogen receptor fusion protein). When the gene expression of ethanol-treated (vehicle) and tamoxifen-treated MEFs was compared at 72 hr post-induction, 83 genes were induced and 111 genes were down-regulated at least 1.5-fold upon inactivation of Hdac3. Approximately, 48 genes were up-regulated in both Ad-Cre and tamoxifen-treated MEFs at the 72 hr time point. The majority of the affected genes were associated with signal transduction and metabolism. Overall, few of the up-regulated genes at the 72hr time point in Ad-Cre and tamoxifen-treated MEFs are associated with apoptosis or with cell cycle control. Thus, these metabolic regulatory genes may be “core” Hdac3-regulated genes, and alterations in gene expression are unlikely to trigger apoptosis. Keywords: Conditional knock out analysis, genetic modification

Dataset Information

The critical roles of histone deacetylase 3 in the pathogenesis of solid organ injury.

Publications

The critical roles of histone deacetylase 3 in the pathogenesis of solid organ injury.

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