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Astrocyte Elevated Gene-1/Metadherin (AEG-1/MTDH) in Myeloid Cells Regulates Metabolic Dysfunction-Associated Steatohepatitis (MASH)

ABSTRACT: Astrocyte elevated gene-1/Metadherin (AEG-1/MTDH) plays an important role in regulating lipid metabolism and inflammation in hepatocytes, and promotes metabolic dysfunction-associated steatohepatitis (MASH). Myeloid cells, such as macrophages, play a key role in regulating inflammation. Here we investigated the role of AEG-1 in myeloid cells in regulating high fat/high sugar diet (HF/HSD)-induced MASH. Both male and female AEG-1MAC mice were significantly protected from MASH development compared to AEG-1fl/fl mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE302723 | GEO | 2026/01/27

REPOSITORIES: GEO

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Similar Datasets

Astrocyte Elevated Gene-1/Metadherin (AEG-1/MTDH) in Myeloid Cells Regulates Metabolic Dysfunction-Associated Steatohepatitis (MASH) [Spatial Transcriptomics]

Project description:Astrocyte elevated gene-1/Metadherin (AEG-1/MTDH) plays an important role in regulating lipid metabolism and inflammation in hepatocytes, and promotes metabolic dysfunction-associated steatohepatitis (MASH). Myeloid cells, such as macrophages, play a key role in regulating inflammation. Here we investigated the role of AEG-1 in myeloid cells in regulating high fat/high sugar diet (HF/HSD)-induced MASH. Both male and female AEG-1MAC mice were significantly protected from MASH development compared to AEG-1fl/fl mice.

2026-01-27 | GSE302842 | GEO

Spatial Transcriptomics Unravels Palmitoylation and Zonation-Dependent Gene Regulation by AEG-1 in Mouse Liver

Project description:Obesity-induced metabolic dysfunction-associated steatohepatitis (MASH) leads to hepatocellular carcinoma (HCC). Astrocyte-elevated gene-1/Metadherin (AEG-1/MTDH) plays a key role in promoting MASH and HCC. AEG-1 is palmitoylated at residue cysteine 75 (Cys75) and a knock-in mouse representing mutated Cys75 to serine (AEG-1-C75S) showed activation of MASH- and HCC-promoting gene signature when compared to wild-type littermates (AEG-1-WT). The liver consists of 3 zones, periportal, midlobular and pericentral, and zone-specific dysregulated gene expression impairs metabolic homeostasis in the liver, contributing to MASH and HCC. Here, to elucidate how palmitoylation influences AEG-1-mediated gene regulation in regards to hepatic zonation, we performed spatial transcriptomics (ST) in the livers of AEG-1-WT and AEG-1-C75S littermates.

2024-06-05 | GSE261057 | GEO

Dissecting the Balance between Metabolic and Oncogenic Functions of Astrocyte Elevated Gene-1/Metadherin (AEG-1/MTDH)

Project description:Obesity is an enormous global health problem and obesity-induced non-alcoholic steatohepatitis (NASH) is contributing to a rising incidence and mortality for hepatocellular carcinoma (HCC). Increase in de novo lipogenesis (DNL) and decrease in fatty acid -oxidation (FAO) underlie hepatic lipid accumulation in NASH. Astrocyte elevated gene-1/metadherin (AEG-1/MTDH) overexpression contributes to both NASH and HCC. AEG-1 harbors an LXXLL motif through which it blocks activation of peroxisome proliferator activated receptor  (PPAR), a key regulator of FAO. To better understand the role of LXXLL motif in mediating AEG-1 function, using CRISPR/Cas9 technology, we have generated a novel mouse model (AEG-1-L24K/L25H) in which the LXXLL motif in AEG-1 was mutated to LXXKH. We observed increased activation of PPAR in AEG-1-L24K/L25H livers providing partial protection from high fat diet (HFD)-induced steatosis. Interestingly, even with equal gene dosage levels, compared to AEG-1-WT livers, AEG-1-L24K/L25H livers exhibited increase in levels of lipogenic enzymes, mitogenic activity and inflammation which are attributes observed when AEG-1 is overexpressed. These findings indicate that while LXXLL motif favors steatotic activity of AEG-1 it keeps in check inflammatory and oncogenic functions thus maintaining a homeostasis in AEG-1 function. Conclusion: AEG-1 is being increasingly appreciated as a viable target for ameliorating NASH and NASH-HCC and as such in-depth understanding of the functions and molecular attributes of this molecule is essential. The present studies unravel the unique role of the LXXLL motif in mediating the balance between the metabolic and oncogenic functions of AEG-1.

2022-03-02 | GSE156849 | GEO

Dissecting the Balance between Metabolic and Oncogenic Functions of Astrocyte Elevated Gene-1/Metadherin (AEG-1/MTDH)

Project description:Dissecting the Balance between Metabolic and Oncogenic Functions of Astrocyte Elevated Gene-1/Metadherin (AEG-1/MTDH)

| PRJNA659367 | ENA

Expression data from metadherin (MTDH) knockdown in the Ishikawa H endometrial cancer cell line

Project description:Understanding the molecular underpinnings of chemoresistance is vital to design therapies to restore chemosensitivity. In particular, metadherin (MTDH) has been demonstrated to have a critical role in chemoresistance. Over-expression of MTDH has recently been implicated in poor clinical outcome in breast cancer, neroblastoma, hepatocellular carcinoma and prostate cancer. In this present study, we focused on the therapeutic benefit of MTDH depletion to restore sensitivity to cell death mediated by a combinatorial therapy of tumor necrosis factor-alpha-related apoptosis-inducing ligand (TRAIL), which promotes death of cancerous cells of the human reproductive tract, and histone deacetylase (HDAC) inhibitors, which have been shown to increase sensitivity of cancer cells to TRAIL-induced apoptosis. Our data indicate that depletion of MTDH in endometrial cancer cells results in sensitization of cells that were previously resistant to cell death mediated by combinatorial treatment with TRAIL and HDAC inhibitor LBH589. MTDH was found to be involved in G2/M checkpoint regulation in response to LBH589 alone or LBH589 in combination with TRAIL, suggesting that MTDH functions at the cell cycle checkpoint to accomplish resistance.Using microarray technology, we identified 57 downstream target genes of MTDH, including Calbindin 1 and Galectin 1, which may contribute to MTDH-mediated resistance to combinatorial TRAIL and HDAC inhibitor targeted therapy. Inhibition of PDK1,AKT phosphorylation and increase Bim expression and XIAP degradation may result in sensitivity to cell death induction in MTDH depleted Hec50co cells by TRAIL and LBH 589 combination treatment. These findings indicate that depletion of MTDH is a potentially novel avenue for effective cancer therapy.

2011-05-01 | GSE27828 | GEO

Expression data from metadherin (MTDH) knockdown in the Ishikawa H endometrial cancer cell line

2011-05-01 | E-GEOD-27828 | biostudies-arrayexpress

AEG-1 silencing induced gene expression alteration in glioma cells

2011-07-12 | GSE29952 | GEO

AEG-1 silencing induced gene expression alteration in glioma cells

Project description:This experiment is designed to evaluate gene expression alteration following AEG-1 (MTDH) silencing in glioma cells. AEG-1 is found to be a potential regulator through interaction with other transcription factor. We intended to investigate the enriched transcription factor dependent downstream gene sets regulated by AEG-1 form the differential expressed genes we obtained from AEG-1 silencing. Total RNA were extracted from U87MG glioma cells stably silencing AEG-1 and correspondent pSuper Retro vector cells respectively. Passage 5 of the indicated cells after infection and selection were harvested for RNA extraction.

2011-07-12 | E-GEOD-29952 | biostudies-arrayexpress

A newly identified spliced isoform of metadherin differently regulates the global transcriptomic profile in MCF-7 breast cancer cells

2014-09-01 | GSE59055 | GEO

A newly identified spliced isoform of metadherin differently regulates the global transcriptomic profile in MCF-7 breast cancer cells

Project description:The current study analyzed the metadherin (MTDH)-mediated altered gene expression profiles in ER positive MCF-7 cells. Some of these altered gene expressions were further inter connected to various pathways which may eventually be recognized as drug targets or biomarkers in those breast cancers where MTDH plays a role in cancer progression/metastasis. To understand the global differential gene expression profile in MTDH-wild type and a newly identified MTDH-isoform knock down in malignant breast cancer cells. This data was compared to untreated breast cancer cells.

2014-09-01 | E-GEOD-59055 | biostudies-arrayexpress

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