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Targeting Epsins by nanotherapy regulates lipid metabolism and promotes ABCG1-mediated cholesterol efflux to fortify atheroma regression [RNA-seq]

ABSTRACT: Targeting Epsins by nanotherapy regulates lipid metabolism and promotes ABCG1-mediated cholesterol efflux to fortify atheroma regression [RNA-seq]

PROVIDER: PRJNA885163 | ENA |

REPOSITORIES: ENA

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Targeting Epsins by nanotherapy regulates lipid metabolism and promotes ABCG1-mediated cholesterol efflux to fortify atheroma regression.

Project description:Targeting Epsins by nanotherapy regulates lipid metabolism and promotes ABCG1-mediated cholesterol efflux to fortify atheroma regression.

| PRJNA885161 | ENA

Targeting Epsins by nanotherapy regulates lipid metabolism and promotes ABCG1-mediated cholesterol efflux to fortify atheroma regression [scRNA-seq]

Project description:Targeting Epsins by nanotherapy regulates lipid metabolism and promotes ABCG1-mediated cholesterol efflux to fortify atheroma regression [scRNA-seq]

| PRJNA885162 | ENA

Targeting Epsins by nanotherapy regulates lipid metabolism and promotes ABCG1-mediated cholesterol efflux to fortify atheroma regression [scRNA-seq]

Project description:Excess cholesterol accumulation in lesional macrophages elicits complex responses in atherosclerosis. Epsins, a family of endocytic adaptors, fuel the progression of atherosclerosis; however, the underlying mechanism and therapeutic potential of targeting Epsins remains unknown. In this study, we determined the role of Epsins in macrophage-mediated metabolic regulation. We then developed an innovative method to therapeutically-target macrophage Epsins with specially-designed S2P-conjugated lipid nanoparticles (NPs), which encapsulate small interfering RNAs to suppress Epsins.Our findings suggest that targeting Epsins in lesional macrophages may offer therapeutic benefits for advanced atherosclerosis by reducing CD36-mediated lipid uptake and increasing ABCG1-mediated cholesterol efflux.

2022-11-26 | GSE214413 | GEO

Targeting Epsins by nanotherapy regulates lipid metabolism and promotes ABCG1-mediated cholesterol efflux to fortify atheroma regression [RNA-seq]

2022-11-26 | GSE214412 | GEO

Targeting Epsins by nanotherapy regulates lipid metabolism and promotes ABCG1-mediated cholesterol efflux to fortify atheroma regression.

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-11-26 | GSE214414 | GEO

Effects of deletioin of cholesterol efflux genes Abca1 and Abcg1 on other gene expressions in macrophages

Project description:ATP binding cassette subfamily member 1 (ABCA1) and G1 (ABCG1) are cholesterol efflux transporter to prevent excess intracellular cholesterol accumulation. We here report the deletion of Abca1 and Abcg1 results in the significant increased expression of Cd38, a multi-faceted ectoenzyme with NADase activity.

2024-04-17 | GSE234507 | GEO

Inflammatory markers in ABCG1-/- lungs

Project description:Transcriptional profiling of cytokines and its receptors in lungs from 8 month old chow-fed wild-type and ABCG1-/- mice Keywords: genotype comparison; inflammatory mediators 4 individual mice per group; RNA from inferior left lobe; WT vs. ABCG1-/-

2010-05-25 | E-GEOD-8976 | biostudies-arrayexpress

Adrenal Abcg1 controls cholesterol flux and steroidogenesis

Project description:Cholesterol is the precursor of all steroids, but how cholesterol flux is controlled in steroidogenic tissues is poorly understood. The cholesterol exporter ABCG1 is an essential component of the reverse cholesterol pathway and its systemic inactivation results in neutral lipid redistribution to macrophages. However, the function of ABCG1 in steroidogenic organs is not explored. To model this question, we inactivated the ortholog Abcg1 gene in the mouse adrenal cortex. Abcg1 disruption led to an adrenal-specific increase in transcripts involved in cholesterol uptake and de novo synthesis, and to an 80% increase in corticosterone production. Importantly, this phenotype was not recapitulated by inactivation of the cholesterol exporter Abca1. The absence of any change in lipid profile suggested that adrenal Abcg1 is not involved in cholesterol export to a clinically relevant extent.

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Effects of deletioin of cholesterol efflux genes Abca1 and Abcg1 on other gene expressions in macrophages

Project description:Effects of deletioin of cholesterol efflux genes Abca1 and Abcg1 on other gene expressions in macrophages

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Lipid Droplet-Associated Hydrolase Mobilizes Oxysterol Stores and Inhibits Atheroma Growth and Progression

Project description:Lipid droplets (LDs) of foam cells within atheroma contain abundant cholesterol, but also serve as reservoirs of central bioactive lipids. The mechanisms of storage and mobilization of many of these lipids remain obscure. LD-associated hydrolase (LDAH) localizes to LDs, has a lipase structure, and is abundant in atheroma. However, its lipid substrates and role in atherogenesis are unknown. Using knockout and transgenic mice we found that LDAH protects against atherosclerosis. Myeloid LDAH expression is sufficient to inhibit lesion progression and promote stable architectures, less necrotic, and richer in fibrillar collagen. Lipidomics coupled with RNA sequencing revealed that LDAH facilitates mobilization of esters of oxysterols that are liver X receptor agonists, leading to induction of cholesterol efflux transporters, reduced foam cell inflammation, and pro-fibrotic gene signatures. These studies identify LDAH as a novel player in neutral hydrolysis of esterified regulatory sterols that promotes atheroprotective and pro-stabilizing mechanisms beyond mass cholesterol removal.

2020-11-10 | GSE157947 | GEO

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