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The receptor tyrosine kinase EphB2 promotes MASH fibrosis in mice.

ABSTRACT: Metabolic dysfunction-associated steatohepatitis (MASH) is emerging as the leading cause for liver transplantation worldwide. MASH is chatacterized by hepatic lipid accumulation, inlammation and fibrosis which is associaed with worst outcome in patients sufferring from this pathology. Using the Gubra Amyln NASH (GAN) diet model of murine MASH, we showed that global deletion of Ephb2 in mice protect them from GAN diet-induced inlammation and fibrosis. EphB2 could be a potential therapeutic target for the treatment of MASH fibrosis.

ORGANISM(S): Mus musculus

PROVIDER: GSE274897 | GEO | 2026/01/31

REPOSITORIES: GEO

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EphB2 deficiency in hepatic stellate cells mitigated MASH fibrosis in mice.

Project description:Metabolic dysfunction-associated steatohepatitis (MASH) is emerging as the leading cause for liver transplantation worldwide. MASH is chatacterized by hepatic lipid accumulation, inlammation and fibrosis which is associaed with worst outcome in patients sufferreing from this pathology. Using the murine choline deficient amino acid defined high fat diet (CDAA-HFD) model of MASH we showed that Ephb2-specific deletion in HSCs using the tamoxifen inducible PdgfCre-eRT2 promoer driver is sufficient to mitigate MASH fibrosis in mice.

2026-01-31 | GSE274899 | GEO

The receptor tyrosine kinase EphB2 promotes MASH fibrosis in mice.

Project description:The receptor tyrosine kinase EphB2 promotes MASH fibrosis in mice.

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Identification of a Broadly Fibrogenic Macrophage Subset Induced by Type 3 Inflammation

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2023-03-27 | GSE228232 | GEO

EphB2 deficiency in hepatic stellate cells mitigated MASH fibrosis in mice.

Project description:EphB2 deficiency in hepatic stellate cells mitigated MASH fibrosis in mice.

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TGF-beta mediated hepatic stellate cells activation is dampened in the absence of EPHB2 in vitro.

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2026-01-31 | GSE274898 | GEO

EphB2 Receptor Promotes Dermal Fibrosis in Systemic Sclerosis

Project description:Objectives: Eph/Ephrin cell-cell signaling is emerging as a key player in tissue fibrogenesis. The aim of this study was to test the hypothesis that the receptor tyrosine kinase EphB2 mediates dermal fibrosis in systemic sclerosis (SSc). Methods: We assessed normal and SSc human skin biopsies for EphB2 expression. The in vivo role of EphB2 in skin fibrosis was investigated by subjecting EphB2-knockout mice to both bleomycin-induced and tight skin (Tsk1/+) genetic mouse models. EphB2 kinase-dead and overactive point mutant mice were used to evaluate the role of EphB2 forward signaling in bleomycin-induced dermal fibrosis. In vitro studies were performed on dermal fibroblasts from SSc patients and healthy controls, which was followed by in vivo analysis of fibroblast-specific EphB2 deficient mice. Results: Expression of EphB2 is upregulated in SSc skin tissue and explanted SSc dermal fibroblasts compared to healthy controls. EphB2 expression is elevated in two animal models of dermal fibrosis. In mice, EphB2 drives dermal fibrosis in both the bleomycin and the Tsk1/+ models of skin fibrosis. EphB2 forward signaling is a critical mediator of dermal fibrosis. Transforming growth factor-β (TGFβ) cytokines upregulate EphB2 in dermal fibroblasts via non-canonical TGFβ/SMAD signaling and silencing EphB2 in dermal fibroblasts is sufficient to dampen TGFβ-induced fibroblast-to-myofibroblast differentiation. Moreover, mice with fibroblast-specific deletion of EphB2 showed impaired fibroblast-to-myofibroblast differentiation and reduced skin fibrosis upon bleomycin challenge. Conclusion: Our data implicate EphB2 overexpression and kinase-mediated forward signaling in the development of dermal fibrosis in SSc. EphB2 thus represents a potential new therapeutic target for SSc.

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Single-nucleus RNA-seq profiling of healthy and MASH mouse livers reveals hepatocyte heterogeneity under MASH condition

Project description:Metabolic dysfunction-associated steatohepatitis (MASH) is a severe chronic liver condition characterized by hepatocyte steatosis, inflammation and fibrosis, with a rising prevalence globally, posing significant health risks and potentially leading to complications such as cirrhosis, liver failure, and increased mortality. To obtain a deeper understanding of transcriptomic responses to MASH diet feeding, we conducted a single-nucleus RNA-seq (snRNA-seq) experiment on livers from mice fed on regular chow or a MASH diet. Our snRNA-seq analysis revealed expansion of cholangiocytes and activated hepatic stellate cells population, as well as infiltration of macrophages in the MASH livers. In addition, we identified a cluster of hepatocytes, termed disease-associated hepatocytes, that are unique to the MASH livers and are distinct from the hepatocytes from the three liver zonations.

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2024-01-16 | GSE246328 | GEO

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Project description:Metabolic dysfunction-associated steatohepatitis (MASH) is a progressive liver disease characterized by steatosis, inflammation, and fibrosis. However, the mechanisms linking lipid droplet (LD) metabolism to MASH progression remain poorly understood. AF6 is a polarity protein known to regulate metabolic homeostasis, but its role in the development of MASH remains largely undefined. Here, we identify AF6 as a critical regulator of hepatic lipid accumulation and inflammation in MASH. Hepatic AF6 expression is elevated in MASH patients and diet-induced mouse models. Liver-specific deletion of AF6 attenuated steatosis, inflammation, and fibrosis in both high-fat, high-cholesterol (HFHC) and choline-deficient, amino acid-defined high-fat diet (CDA-HFD)-induced MASH models. Mechanistically, lipid overload promotes nuclear translocation of AF6, which interacts with the transcription factor C/EBPβ and enhances its nuclear accumulation. This interaction increases transcription of the lipid droplet fusion protein CIDEA, promoting LD growth and lipid deposition. AF6 also exacerbates MASH by enhancing C/EBPβ-mediated proinflammatory signaling. Restoration of CIDEA expression in AF6-deficient mice reverses the protective effects. In human liver biopsies and iPSC-derived liver organoids, the AF6–C/EBPβ–CIDEA axis is upregulated and correlates with disease severity. Importantly, a CRISPR-Cas9–based lipid nanoparticle (LNP) therapy targeting AF6 effectively reduced lipid accumulation, inflammation, and fibrosis in MASH mice and organoids. AF6 promotes MASH progression by facilitating C/EBPβ nuclear localization and transcriptional activation of CIDEA. Targeting the AF6–C/EBPβ–CIDEA axis represents a promising therapeutic strategy for treating MASH.

2026-02-18 | GSE305662 | GEO

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