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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE208641 | 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 II

Project description: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.

2024-02-02 | GSE208705 | 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.

2024-02-02 | GSE234244 | GEO

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.

2024-02-02 | GSE208706 | GEO

Administration of glutaredoxin-1 attenuates liver fibrosis caused by aging and non-alcoholic steatohepatitis

Project description:Glutaredoxin-1 (Glrx) controls redox signaling and has an anti-apoptotic function. We evaluated the role of Glrx on hepatic cell damage and fibrosis induced by a high-fat diet. We fed mice a high-fat high-fructose diet to induce non-alcoholic steatohepatitis (NASH) and injected AAV-Glrx to express hepatocyte-specific Glrx in diet-induced NASH mice. AAV-Glrx suppressed fibrosis and improved liver function in the NASH liver. We used microarrays to profile gene expression in the NASH liver and find pathways that AAV-Glrx mediated to attenuate fibrosis and NASH progression.

2022-06-01 | GSE198961 | GEO

Amphiregulin activates human hepatic stellate cells and is upregulated in non alcoholic steatohepatitis.

Project description:Amphiregulin (AR) involvement in liver fibrogenesis and hepatic stellate cells (HSC) regulation is under study. Non-alcoholic fatty liver disease (NAFLD) and its more severe form non-alcoholic steatohepatitis (NASH) may progress to cirrhosis and hepatocellular cancer (HCC). Our aim was to investigate ex vivo the effect of AR on human primary HSC (hHSC) and verify in vivo the relevance of AR in NAFLD fibrogenesis. hHSC isolated from healthy liver segments were analyzed for expression of AR and its activator, TNF-α converting enzyme (TACE). AR induction of hHSC proliferation and matrix production was estimated in the presence of antagonists. AR involvement in fibrogenesis was also assessed in a mouse model of NASH and in humans with NASH. hHSC time dependently expressed AR and TACE. AR increased hHSC proliferation through several mitogenic signaling pathways such as EGFR, PI3K and p38. AR also induced marked upregulation of hHSC fibrogenic markers and reduced hHSC death. AR expression was enhanced in the HSC of a murine model of NASH and of severe human NASH. In conclusion, AR induces hHSC fibrogenic activity via multiple mitogenic signaling pathways, and is upregulated in murine and human NASH, suggesting that AR antagonists may be clinically useful anti-fibrotics in NAFLD.

| S-EPMC4351520 | biostudies-other

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.

2022-10-21 | GSE212837 | GEO

Single Cell Landscape of Left Atria Reveals Amphiregulin and Insulin-like Growth Factor 1 as Surrogate Markers in Patients with Atrial Fibrillation.

Project description:Atrial fibrillation (AF) is strongly associated with strokes, heart failure, and increased mortality. Inflammation plays a role in the pathophysiology of AF; however, how inflammation in AF is sustained and induces fibrosis is unclear. Therefore, this study aimed to identify the characteristic monocyte–macrophage heterogeneity and the cell–cell interactions between immune and non-immune cells at a single cell level in the left atrial (LA) tissues of patients with AF who underwent LA appendectomies. Myeloid cells were divided into five macrophage clusters, TNF+, two IL1B+, TREM2+, LYVE1+ resident macrophages, three monocyte clusters, five dendritic cell clusters, neutrophils, and mast cells. The CellChat analysis revealed that IL1B+ macrophages send epidermal growth factor (EGF) signalling to fibroblasts and resident macrophages send IGF1 singalling to cardiomyocytes. When compared to openly published control samples, Amphiregulin (AREG) was the most upregulated gene in monocytes and monocyte-derived IL1B+ macrophages in the AF group. We also found that AREG levels in serum were higher in patients with AF than controls. EGF signalling from IL1B+ macrophages could be therapeutic targets for AF, and AREG could be a functional biomarker for AF.

2024-06-01 | GSE261170 | GEO

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

Effect of Amphiregulin on global gene expression in injured skeletal muscle in the presence or absence of CD4+Foxp3+ regulatory T cells (Tregs).

Project description:Global gene expression analysis of injured skeletal muscle showed that amphiregulin (Areg), a growth factor over-expressed by muscle Treg cells, enhances muscle regeneration both in the presence and in the absence of Tregs.

2013-12-15 | GSE50097 | GEO

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