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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

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

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

| PRJNA860635 | ENA

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

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

| PRJNA860529 | ENA

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

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

| PRJNA860637 | ENA

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

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

| PRJNA980619 | ENA

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

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

| PRJNA979265 | ENA

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

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