E-MTAB-9864
Ontology highlight
ABSTRACT:
PROVIDER: E-MTAB-9864 | ExpressionAtlas | 2020-12-11
REPOSITORIES: ExpressionAtlas
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Project description:INSIG1 in NASH pathophysiology and in the hepatic wound-healing response
| PRJEB41800 | ENA
Project description:We investigated the biological function of INSIG1 in acute (CCl4) and chronic (NASH) liver damage. Male whole-body Insig1 wild-type (WT), Heterozygous (HET) and Knock-out (KO) mice were: 1) challenged with Olive Oil or CCl4 single IP injection and sacrificed 4 days after the treatment; 2) fed Low Fat Diet (LFD) or Western Diet plus Sugar Water (WDSW) and sacrificed after 12 weeks of the challenge. Hepatic RNA was extracted and studied by Next Generation Sequencing to highlight changes in the transcriptome driven by the challenges and genotype-associated differences.
2021-04-14 | E-MTAB-9864 | biostudies-arrayexpress
Project description:RNA-seq of liver from pigs divergent in feed efficiency highlights shifts in macronutrients metabolism, hepatic growth and immune response
2020-07-23 | E-MTAB-6256 | ExpressionAtlas
Project description:Investigating multigenerational epigenetic adaptation of the hepatic wound-healing response
| PRJNA954835 | ENA
Project description:The possibility that ancestral environmental conditions and exposures could result in effects inherited across generations, with potential impact for human health, has been long debated. Here, we comprehensively investigate transgenerational effects of the hepatotoxicant carbon tetrachloride (CCl4) on the hepatic wound-healing response in male rats. Detailed microscopic and clinical pathology evaluations do not support adaptive phenotypic suppression of the hepatic wound-healing response or a greater fitness of animals with ancestral liver injury exposure as originally reported. We produced RNAseq libraries on the F2 liver samples to further characterize any adaptive effect based on molecular changes.
2023-09-06 | GSE229524 | GEO
Project description:Liver fibrosis is a reversible wound-healing response to liver injury and hepatic stellate cells (HSCs) are central cellular players that mediate hepatic fibrogenesis. However, the molecular mechanisms that govern this process remain unclear. Here, we reveal a novel cistromic circuit in HSCs comprising the vitamin D receptor (VDR) and SMAD transcription factors that restrains the intensity of hepatic fibrogenesis. Ligand-activated VDR suppresses TGFβ1-induced pro-fibrotic gene expression in HSCs. Administration of a vitamin D analogue, calcipotriol, diminishes the fibrotic response in a mouse model of liver fibrosis, while VDR knockout mice spontaneous develop extensive hepatic fibrosis by age 6 months. Using ChIP-Seq, we find that the anti-fibrotic properties of VDR are due to crosstalk with SMAD, mediated by their co-occupancy of DNA-binding sites on pro-fibrotic genes. Specifically, SMAD binding potentiates local chromatin accessibility to enhance VDR recruitment at the same cis-regulatory elements, which reciprocally antagonizes the interaction between SMAD3 and chromatin and limits the assembly of transcriptional activation complexes at fibrotic genes, a process that is enhanced by the presence of VDR agonists. These results not only establish this coordinated VDR/SMAD cistromic circuit as a master regulator of hepatic fibrogenesis, but also support VDR as a potential drug target to ameliorate liver fibrosis. Identification of VDR, SMAD3 and H3 binding sites in human stellate LX2 cells that were pre-treated with calcipotriol (100nM) for 16 hrs (where calcipotriol treatment is indicated) followed by incubation of calcipotriol (100nM) or TGFβ1 (1ng/ml) for another 4 hours (where indicated).
2013-04-29 | E-GEOD-38103 | biostudies-arrayexpress
Project description:Hepatic fibrosis is caused by liver damage as a consequence of wound healing response. Recent studies have shown that hepatic fibrosis could be effectively reversed, partly through regression of activated hepatic stellate cells (HSCs). Transcription factor 21 (TCF21), a member of the basic helix-loop-helix (bHLH) transcription factor, is involved in epithelial-mesenchymal transformation in various diseases. However, the mechanism by which TCF21 regulates epithelial-mesenchymal transformation in hepatic fibrosis has not been elucidated. In this research, we found that hnRNPA1, the downstream binding protein of TCF21, accelerates liver fibrosis reversal by inhibiting the NF-κB signaling pathway. Furthermore, the combination of DNMT3a with TCF21 promoter results in TCF21 hypermethylation. Our results suggest that DNMT3a regulation of TCF21 is a significant event in reversing hepatic fibrosis. In conclusion, this research identifies a novel signaling axis, DNMT3a-TCF21-hnRNPA1, that regulates HSCs activation and liver fibrosis reversal, providing a novel treatment strategy for hepatic fibrosis.
2024-10-01 | GSE232674 | GEO
Project description:Transcriptomic profiling of mutant and WT HNF4alpha hepatic progenitor stage cells
2025-01-23 | E-MTAB-7951 | ExpressionAtlas
Project description:Liver fibrosis is a reversible wound-healing response to liver injury and hepatic stellate cells (HSCs) are central cellular players that mediate hepatic fibrogenesis. However, the molecular mechanisms that govern this process remain unclear. Here, we reveal a novel cistromic circuit in HSCs comprising the vitamin D receptor (VDR) and SMAD transcription factors that restrains the intensity of hepatic fibrogenesis. Ligand-activated VDR suppresses TGFβ1-induced pro-fibrotic gene expression in HSCs. Administration of a vitamin D analogue, calcipotriol, diminishes the fibrotic response in a mouse model of liver fibrosis, while VDR knockout mice spontaneous develop extensive hepatic fibrosis by age 6 months. Using ChIP-Seq, we find that the anti-fibrotic properties of VDR are due to crosstalk with SMAD, mediated by their co-occupancy of DNA-binding sites on pro-fibrotic genes. Specifically, SMAD binding potentiates local chromatin accessibility to enhance VDR recruitment at the same cis-regulatory elements, which reciprocally antagonizes the interaction between SMAD3 and chromatin and limits the assembly of transcriptional activation complexes at fibrotic genes, a process that is enhanced by the presence of VDR agonists. These results not only establish this coordinated VDR/SMAD cistromic circuit as a master regulator of hepatic fibrogenesis, but also support VDR as a potential drug target to ameliorate liver fibrosis.
2013-04-29 | GSE38103 | GEO
Project description:The gut microbiota promotes hepatic fatty acid desaturation and elongation in mice
2018-09-17 | E-MTAB-6079 | ExpressionAtlas