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Gene expression profiling of HDAC3-depleted mouse liver rescued with wild-type exogenous HDAC3

ABSTRACT: We have shown that intravenous injection of HDAC3 floxed mice with adeno-associated virus (AAV) expressing Cre depletes hepatic HDAC3, upregulates lipogenic gene expression, and causes fatty liver. When AAV-Flag-HDAC3 wild-type (WT) is co-injected along with AAV-Cre, the exogenous HDAC3 is expressed at endogenous levels and can completely rescue fatty liver phenotype. Here we profile transcriptome of the rescued WT livers in comparison with HDAC3-depleted (KO) livers.

ORGANISM(S): Mus musculus

PROVIDER: GSE49386 | GEO | 2013/11/25

SECONDARY ACCESSION(S): PRJNA213911

REPOSITORIES: GEO

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Gene expression profiling of HDAC3-depleted mouse liver rescued with wild-type exogenous HDAC3

Project description:We have shown that intravenous injection of HDAC3 floxed mice with adeno-associated virus (AAV) expressing Cre depletes hepatic HDAC3, upregulates lipogenic gene expression, and causes fatty liver. When AAV-Flag-HDAC3 wild-type (WT) is co-injected along with AAV-Cre, the exogenous HDAC3 is expressed at endogenous levels and can completely rescue fatty liver phenotype. Here we profile transcriptome of the rescued WT livers in comparison with HDAC3-depleted (KO) livers. 4-months old C57BL/6 male mice were co-injected with AAV-Cre or AAV-Cre plus AAV-Flag-HDAC3. Mice were fed ad libitum and harvested at 5 pm (ZT10) at 2-weeks post-injection. Liver total RNA was extracted and hybridized to Affymetrix Mouse Gene 1.0ST array.

2013-11-25 | E-GEOD-49386 | biostudies-arrayexpress

Genome-wide acetylated histone 3 lysine 9 (H3K9ac) in HDAC3-depleted liver rescued with deacectylase-dead HDAC3 mutants

Project description:We found that several deacetylase-dead HDAC3 mutants were able to rescue the metabolic phenotype of HDAC3-depleted livers. Here we profile the histone acetylation in the presence of different HDAC3 mutants in mouse liver. Deacetylase-dead HDAC3 mutants, including HAHA, KA, YF and HEBI, were introduced into HDAC3-depleted (Cre) mouse livers by virus along with wild-type (WT) HDAC3 as a control. Livers were harvested at 5 pm (ZT 10) and subjected to ChIP with anti-H3K9ac antibodies followed by deep sequencing.

2013-11-25 | E-GEOD-49365 | biostudies-arrayexpress

Gene expression in mouse liver depleted of HDAC3

Project description:Liver-specific depletion of HDAC3 leads to liver steatosis (fatty liver), suggesting disregulation of lipid metabolism. This is correlated with changes in lipid metabolic gene expression. Livers depleted of HDAC3 were removed from 12 week old male HDAC3 fl/fl mice (loxP sites flanking exon 4 to 7 of the HDAC3 gene encoding the catalytic domain of HDAC3) one week after the injection of AAV2/8-Tbg-Cre virus. Livers from the HDAC3 fl/fl mice injected with AAV2/8-Tbg-GFP were used as normal controls. mRNA was extracted from 100mg mouse liver samples and hybridized to Affymetrix microarrays. For each group (HDAC3 depleted liver and normal liver), we have 5 samples from different mice.

2011-03-11 | E-GEOD-25937 | biostudies-arrayexpress

Gene expression in mouse liver depleted of HDAC3

2011-03-11 | GSE25937 | GEO

Genome-wide acetylated histone 3 lysine 9 (H3K9ac) in HDAC3-depleted liver rescued with deacectylase-dead HDAC3 mutants

2013-11-25 | GSE49365 | GEO

Nuclear Receptor Corepressors are Required for the Histone Deacetylase Activity of HDAC3 In Vivo (ChIP-Seq)

Project description:We report the genomic regions enriched in Histone Deacetylase 3 (HDAC3) in mouse livers. We also report the change of HDAC3 occupancy upon DAD mutations in NCOR and SMRT. HDAC3 enriched genomic regions in WT and NS-DADm mice livers using Illumina GAIIx.

2013-01-01 | E-GEOD-42540 | biostudies-arrayexpress

Identification of transcriptional changes due to loss of Hdac3 in liver at P17 and P28

Project description:Histone deacetylase 3 (Hdac3) is the enzymatic component of transcriptional repression complexes recruited by the nuclear hormone receptors. Inactivation of Hdac3 in cancer cell lines triggered apoptosis, and removal of Hdac3 in the germ-line of mice caused embryonic lethality. Therefore, we conditionally deleted the Hdac3 allele in the mouse liver. These mice developed hepatomegaly, which was the result of hepatocyte hypertrophy, and these morphological changes coincided with significant imbalances between carbohydrate and lipid metabolism. Loss of Hdac3 triggered changes in gene expression consistent with inactivation of repression mediated by nuclear hormone receptors. Mechanistically, loss of Hdac3 increased the levels of Pparγ2, and treatment of these mice with a Pparγ antagonist partially reversed the lipid accumulation in the liver. In addition, gene expression analysis identified mTOR (mammalian target of rapamycin) signaling as being activated by deletion of Hdac3, and inhibition by rapamycin also affected the accumulation of neutral lipids in the Hdac3-null livers. Thus, Hdac3 has a key role in regulation of multiple signaling pathways in the liver, and deletion of Hdac3 disrupts normal metabolic homeostasis. Keywords: Genetic knockout of Hdac3 specifically in liver, and RNA analyzed from postnatal day 17 or 28 livers for transcriptional changes related to the given phenotypes

2008-05-22 | GSE10503 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of three groups from mouse liver Transcriptomes

Project description:Liver mRNA profiles of WT liver(WT1-WT3) and Alb-Cre:Hdac3−/− liver (0d(Ha-Hc), 7d(Hd-Hg), 21d(Hh-Hk), 50d(Hl-Hn)) receiving successive PH(sPH), Alb-Cre:Hdac3−/− tumor tissues(HCC1-HCC3) and adjacent non-tumor tissues(N1-N3), spontaneous liver cancers of Alb-Cre:Hdac3-/- mice (HCC1-HCC3) and liver tumor of recipient Fah-/- mice (HCCa-HCCc) were generated by deep sequencing.

2021-05-11 | GSE114503 | GEO

Expression data from mouse heart deficient of HDAC3

Project description:Gene expression changes in the heart of MCH3-KO mouse (HDAC3 f/f, Muscle Creatine Kinase-Cre) versus control WT mouse (HDAC3 f/f). Histone deacetylases (HDACs) play important roles in cardiac development and function. We show here that mice deficient of HDAC3 in heart and skeletabl muscle are relatively normal on normal chow, but develop hypertrophic cardiomyopathy and heart failure that leads to death on high-fat diet. This microarray experiment is to explore the underlying molecular mechanism. Hearts from 6-weeks old WT and MCH3-KO C57BL/6 mice (n=4 in each group, male) on normal chow were subjected to RNA extraction and Affymetrix Mouse Gene 1.0ST analysis.

2011-09-20 | E-GEOD-31251 | biostudies-arrayexpress

Enhancers contribute to Hdac3-regulated RNA polymerase recruitment to the promoter-proximal region [PRO-seq]

Project description:HDAC3 is known to repress gene transcription, however, whether it directly regulates transcription initiation or elongation is still under debate. We generated a PRO-seq dataset derived from WT and Hdac3 KO mouse livers and used NRSA to explore the functional role of Hdac3 in transcriptional regulation. We reported that the deletion of Hdac3 caused a global accumulation of transcription in promoter-proximal regions and enhancer regions.

2018-07-31 | GSE111447 | GEO

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