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Expression data from HepG2 (liver hepatocellular cells)

ABSTRACT: In order to identify the effects of ATP7B H1069Q overexpression on the liver transcriptome, we performed Affymetrix GeneChip hybridization experiments. Transcriptome analysis of the hepatocytes overexpressing ATP7B H1069Q, compared with hepatocytes overexpressing ATP7B WT.

ORGANISM(S): Homo sapiens

PROVIDER: GSE51818 | GEO | 2015/07/31

SECONDARY ACCESSION(S): PRJNA225481

REPOSITORIES: GEO

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Expression data from HepG2 (liver hepatocellular cells)

Project description:In order to identify the effects of ATP7B H1069Q overexpression on the liver transcriptome, we performed Affymetrix GeneChip hybridization experiments. Transcriptome analysis of the hepatocytes overexpressing ATP7B H1069Q, compared with hepatocytes overexpressing ATP7B WT. For the analysis on the hepatocytes overexpressing ATP7B H1069Q, total RNA was extracted from HepG2 cells; RNA extracted from hepatocytes overexpressing ATP7B WT was used as control.

2015-07-31 | E-GEOD-51818 | biostudies-arrayexpress

Transcriptome profile of HepG2-expressing ATP7B-H1069Q (liver hepatocellular cells) exposed to JNK or p38 Inhibitor

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Expression data from injected mice overexpressing TFEB specifically in liver

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Expression data from transgenic mice overexpressing TFEB specifically in liver

Project description:In order to identify the effects of TFEB overexpression on liver transcriptome, we performed Affymetrix Gene-Chip hybridization experiments for transgenic mice at P9 Transcriptome analysis of transgenic mice overexpressing TFEB specifically in liver

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Expression data from injected mice overexpressing TFEB specifically in liver

Project description:In order to identify the effects of transcription factor EB (TFEB) overexpression on the liver transcriptome, we performed Affymetrix GeneChip hybridization experiments on injected mice overexpressing TFEB specifically in the liver. For the analysis of the injected mice overexpressing TFEB, total RNA was extracted from the liver of three mice. RNA extracted from the liver of 3 not-injected mice was used as a control.

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Specific changes of liver transcriptome in the early stages of copper accumulation in the mouse model of wilson disease

Project description:Wilson disease (WD) is a severe metabolic disorder caused by genetic inactivation of copper-transporting ATPase ATP7B. In WD, copper accumulates in several tissues, particularly in the liver, inducing marked time-dependent pathological changes. To identify initial events in the copper-dependent development of liver pathology we utilized the Atp7b-/- mice, an animal model for WD. Analysis of mRNA from livers of control and Atp7b-/- 6 weeks-old mice using oligonucleotide arrays revealed specific changes of the transcriptome at this stage of copper accumulation. Few messages (29 up-regulated and 46 down-regulated) change their abundance more than 2-fold pointing to the specific effect of copper on gene expression/mRNA stability. The gene ontology analysis revealed copper effects on distinct metabolic pathways. Keywords: comparative genomic hybridization

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ATP7B Gene Therapy of Autologous Reprogrammed Hepatocytes Alleviates Copper Accumulation in a Murine Model of Wilson’s Disease

Project description:Purpose：Wilson's disease (WD) is a rare hereditary disorder due to ATP7B gene mutation, causing pathologic copper storage mainly in the liver and neurological systems. Hepatocyte transplantation showed therapeutic potential, however, this strategy is often hindered by a shortage of quality donor cells and by allogeneic immune rejection. Here we evaluate the function and efficacy of autologous reprogrammed, ATP7B gene-restored hepatocytes using a murine model of WD Mathods and Results: By reprogramming hepatocytes from ATP7B-/- mice with small molecules, sufficient liver progenitor cells (LPCs) are harvested. After lentivirus-mediated miniATP7B gene transfection and re-differentiation, functional LPC-ATP7B-Heps are developed. RNA-seq data show that compared with LPC-GFP-Heps with enrichment of genes mainly in pathways of oxidative stress and cell apoptosis, in LPC-ATP7B-Heps under high copper stress pathways for copper ion binding and cell proliferation are enriched. LPC-ATP7B-Heps transplantation into ATP7B-/- mice alleviates deposition of excess liver copper with its associated inflammation and fibrosis, comparable to those observed using normal primary hepatocytes at four months after transplantation. Conclusion: We establish the autologous reprogrammed, ATP7B gene restored LPC-ATP7B-Heps and further transplantation demonstrate alleviated copper accumulation in WD mice.

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