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Amphiregulin from regulatory T cells promotes liver fibrosis and insulin resistance in non-alcoholic steatohepatitis II

ABSTRACT: We study the effect of Treg cell-derived Areg on hepatic stellate cells. Here we look at the transcriptional effect of Areg on hepatic stellate cells in vitro.

ORGANISM(S): Mus musculus

PROVIDER: GSE208705 | GEO | 2024/02/02

REPOSITORIES: GEO

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Amphiregulin from regulatory T cells promotes liver fibrosis and insulin resistance in non-alcoholic steatohepatitis [scHSC]

Project description:We study the effect of Treg cell-derived Areg in chronic liver injury. Here we look at the transcriptional changes of hepatic stellate cells in NASH in response to Treg cell-derived Areg.

2024-02-02 | GSE234073 | GEO

Amphiregulin from regulatory T cells promotes liver fibrosis and insulin resistance in non-alcoholic steatohepatitis [scTreg]

Project description:We study the effect of Treg cell-derived Areg in chronic liver injury. Here we look at the transcriptional changes of Treg cells in NASH compared to normal chow.

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Amphiregulin from regulatory T cells promotes liver fibrosis and insulin resistance in non-alcoholic steatohepatitis I

Project description:We study the effect of Treg cell-derived Areg in chronic liver injury. Here we look at the transcriptional changes of Treg cells in fibrosis compared to control and conventional T cells in vivo.

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Amphiregulin from regulatory T cells promotes liver fibrosis and insulin resistance in non-alcoholic steatohepatitis

Project description:This SuperSeries is composed of the SubSeries listed below.

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An autocrine signaling circuit in hepatic stellate cells underlies advanced fibrosis in non-alcoholic steatohepatitis

Project description:Advanced hepatic fibrosis, driven by the activation of hepatic stellate cells (HSCs), affects millions world-wide and is the strongest predictor of mortality in non-alcoholic steatohepatitis (NASH), yet there are no approved anti-fibrotic therapies. To identify novel anti-fibrotic drug targets, we integrated progressive transcriptomic and morphological responses that accompany HSC activation in advanced disease using single nuclear RNA sequencing and tissue clearing in a robust, murine NASH model. In advanced fibrosis, an autocrine HSC signaling circuit emerges that is comprised of 68 receptor-ligand interactions conserved between murine and human NASH. These predicted interactions are supported by the parallel appearance of markedly increased direct stellate cell-cell contacts in murine NASH. As proof of principle, pharmacological inhibition of one such autocrine interaction, NTRK3-NTF3, inhibits human HSC activation in culture and reverses advanced murine NASH-fibrosis in vivo. We have uncovered a novel repertoire of previously uncharacterized anti-fibrotic drug targets underlying advanced fibrosis in vivo. The findings suggest a novel therapeutic paradigm in which stage-specific therapies could yield enhanced anti-fibrotic efficacy in patients with advanced fibrosis.

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Inhibition of Enhancer of Zeste Homologue 2 attenuates TGF-β dependent hepatic stellate cell activation and liver fibrosis

Project description:We report the effect of TGFβ vs PDGF 2h treatment in hepatic stellate cells. We also report the effect of TGFβ treatment for 48h in human hepatic stellate cells.

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Amphiregulin mediates non-cell-autonomous effect of senescence on reprogramming

Project description:Cellular senescence is an irreversible growth arrest with a highly dynamic secretome, termed the senescence-associated secretory phenotype (SASP). Senescence has been implicated in somatic reprogramming to pluripotency. The cell-intrinsic proliferation arrest is a barrier for reprogramming, whereas the SASP facilitates the cell fate conversion in nonsenescent cells. However, the mechanisms by which reprogramming-induced senescence regulates cell plasticity are not well understood. Here, we have further investigated how the heterogeneity of paracrine senescence impacts reprogramming. We show that senescence promotes in vitro reprogramming in a stress-dependent manner. We identified a catalog of SASP factors and pathways potentially involved in the cell fate conversion using an unbiased proteomic analysis. Amphiregulin (AREG), a growth factor frequently secreted by the senescent cells, promotes in vitro reprogramming by accelerating proliferation and MET via the EGFR signaling pathway. Of note, AREG treatment diminished the negative effect of donor age on reprogramming. Finally, AREG enhances in vivo reprogramming in the skeletal muscle. Hence, senescence could facilitate cellular plasticity via various SASP factors to promote reprogramming and tissue repair.

2022-07-28 | PXD028590 | Pride

Deactivation of Hepatic Stellate Cells during Liver Fibrosis Resolution in Mice

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Sex differences in Non-Alcoholic Steatohepatitis (NASH) in mice evoked by a fructose-palmitate-cholesterol (FPC)-enriched diet [single_nucleus]

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