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Spatial transcriptomic profiling of gene expression alterations following ACBP/DBI inhibition in a MASH-Driven HCC mouse model

ABSTRACT: Spatial transcriptomic profiling of gene expression alterations following ACBP/DBI inhibition in a MASH-Driven HCC mouse model

PROVIDER: PRJNA1259950 | ENA |

REPOSITORIES: ENA

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Spatial transcriptomic profiling of gene expression alterations following ACBP/DBI inhibition in a MASH-Driven HCC mouse model

Project description:We identified ACBP/DBI as a critical regulator in the pathogenesis of hepatocellular carcinoma (HCC), with its inhibition significantly impairing hepatocarcinogenesis in MASH-driven HCC models. To further elucidate the underlying transcriptional mechanisms, we performed spatial transcriptomic analyses using formalin-fixed, paraffin-embedded (FFPE) liver tissues from the following two experimental models: (i) Western diet (WD) and CCl₄-treated mice with tamoxifen-inducible ACBP/DBI knockout (Dbi⁻/⁻ mice), with Dbi⁺/⁺ littermates serving as controls, after a total of 27 weeks; (ii) WD and CCl₄-treated mice immunized with either keyhole limpet hemocyanin (KLH) alone or KLH-ACBP conjugate, after a total of 34 weeks.

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Charaterization of potential roles and mechanisms of ACBP/DBI in NASH/MASH-dirven HCC mouse models

Project description:We demonstrated that ACBP/DBI inhibition impaired hepatocarcinogenesis in NASH/MASH-driven HCC models. To further investigate its potential mechanisms at transcriptional level in NASH/MASH-driven HCC models, we performed Bulk RNA-seq analyses with liver tissues from the following three models, namely, (i) WD/CCl4 with tamoxifen inducible ACBP/DBI knout mice (Dbi-/- mice, Dbi+/+ mice as control) for in total 27 weeks; (ii) WD/CCl4 with KLH/KLH-ACBP immunized mice for in total 34 weeks; and (iii) HFD/DEN with KLH/KLH-ACBP immunized miceI for a total of 36 weeks.

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Charaterization of potential roles and mechanisms of ACBP/DBI in NASH/MASH-dirven HCC mouse models

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Supplementation of ACBP/DBI for the Experimental Treatment of Anorexia Nervosa

Project description:Total liver RNA extracts from adult female mice (8-week-old) subjected to CRS (chronic restraint stress) or CDDP (cisplatin) induced anorexia with or without ACBP/DBI delivery to investigate the impact of ACBP/DBI on anorexia-induced transcriptomic alterations.

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Implication of Acyl Coenzyme A Binding Protein (ACBP) in Cushing Syndrome

Project description:Acyl coenzyme A binding protein (ACBP), encoded by the diazepam binding protein (DBI) gene, plays a pivotal role in stimulating appetite and lipo-anabolic reactions, showing correlations with laboratory indications of metabolic syndrome in ostensibly healthy individuals. In a screening effort targeting inhibitors of ACBP/DBI expression among distinct neuroendocrine factors, we discovered that glucocorticoids induce ACBP/DBI secretion in cultured cells. In mouse models of iatrogenic Cushing syndrome, antibody-mediated neutralization of ACBP/DBI prevented the metabolic consequences of prolonged glucocorticoid administration. Our findings suggest that a surge in extracellular ACBP/DBI may mediate crucial aspects of Cushing syndrome.

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Supplementation of ACBP/DBI for the Experimental Treatment of Anorexia Nervosa

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Project description:ACBP/DBI protein neutralization for the experimental treatment of fatty liver disease

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