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VEGF-B Signaling Impairs Endothelial Glucose Transcytosis via an LDLR-dependent Decrease in Membrane Cholesterol Loading [mouse heart]

ABSTRACT: VEGF-B Signaling Impairs Endothelial Glucose Transcytosis via an LDLR-dependent Decrease in Membrane Cholesterol Loading [mouse heart]

PROVIDER: PRJNA609315 | ENA |

REPOSITORIES: ENA

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VEGF-B Signaling Impairs Endothelial Glucose Transcytosis via an LDLR-dependent Decrease in Membrane Cholesterol Loading

Project description:VEGF-B Signaling Impairs Endothelial Glucose Transcytosis via an LDLR-dependent Decrease in Membrane Cholesterol Loading

| PRJNA609312 | ENA

VEGF-B Signaling Impairs Endothelial Glucose Transcytosis via an LDLR-dependent Decrease in Membrane Cholesterol Loading [HBMEC]

Project description:VEGF-B Signaling Impairs Endothelial Glucose Transcytosis via an LDLR-dependent Decrease in Membrane Cholesterol Loading [HBMEC]

| PRJNA609314 | ENA

VEGF-B Signaling Impairs Endothelial Glucose Transcytosis via an LDLR-dependent Decrease in Membrane Cholesterol Loading [HBMEC]

Project description:Regulation of endothelial nutrient transport is poorly understood. Vascular endothelial growth factor (VEGF)-B signaling in endothelial cells promotes uptake and transcytosis of fatty acids (FA) from the bloodstream to the underlying tissue, advancing pathological lipid accumulation and lipotoxicity in diabetic complications. Here we demonstrate a VEGF-B dependent obstruction of endothelial glucose transport attributed to plasma membrane lipid alterations affecting glucose transporter 1 function, which was independent of FA uptake. Specifically, VEGF-B signaling impaired recycling of low-density lipoprotein receptor to the plasma membrane, leading to reduced cholesterol uptake and membrane cholesterol loading, decreasing endothelial glucose uptake capacity. Inhibiting VEGF-B in vivo was accordingly linked to reconstitution of membrane cholesterol and induction of glucose uptake, of particular relevance for conditions inferring insulin resistance and diabetic complications. In summary, our study reveals a novel mechanism of action for VEGF-B in endothelial nutrient uptake and highlights the impact of membrane cholesterol for the regulation of endothelial glucose transport.

2020-04-06 | GSE146108 | GEO

VEGF-B Signaling Impairs Endothelial Glucose Transcytosis via an LDLR-dependent Decrease in Membrane Cholesterol Loading [mouse heart]

2020-04-06 | GSE146107 | GEO

VEGF-B Signaling Impairs Endothelial Glucose Transcytosis via an LDLR-dependent Decrease in Membrane Cholesterol Loading

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

2020-04-06 | GSE146109 | GEO

VEGF-D deficiency causes hyperlipidemia and delayed clearance of chylomicron remnants

Project description:Objective: Dyslipidemia is one of the key factors behind coronary heart disease. Blood and lymphatic vessels play pivotal roles in both lipoprotein metabolism and development of atherosclerotic plaques. Recent studies have linked members of Vascular Endothelial Growth Factor (VEGF) family to lipid metabolism but the function of VEGF-D has remained unexplored. Here we investigated how the deletion of VEGF-D affects lipid and lipoprotein metabolism in atherogenic LDLR-/-ApoB100/100 mice. Approach and Results: Deletion of VEGF-D (Vegfd-/-LDLR-/-ApoB100/100) led to markedly elevated plasma cholesterol and triglyceride levels without an increase in atherogenesis. Size distribution and hepatic lipid uptake studies confirmed a delayed clearance of large chylomicron remnant particles that cannot easily penetrate through the vascular endothelium. Mechanistically, the inhibition of VEGF-D signaling significantly decreased the hepatic expression of syndecan 1 (SDC1), which is one of the main receptors for chylomicron remnant uptake when LDLR is absent. Immunohistochemical staining confirmed reduced expression of SDC1 in the sinusoidal surface of hepatocytes in VEGF-D deficient mice. Furthermore, hepatic RNA sequencing revealed that VEGF-D is also an important regulator of genes related to lipid metabolism and inflammation. The lack of VEGF-D signaling via VEGF receptor 3 led to lowered expression of genes regulating triglyceride and cholesterol production as well as downregulation of peroxisomal β-oxidation pathway. Conclusions: These results demonstrate that VEGF-D, a powerful lymphangiogenic and angiogenic growth factor, is also a major regulator of chylomicron metabolism in mice.

2018-08-16 | GSE108959 | GEO

Single-nucleus RNA-seq of aortas from Ldlr-/- and Ldlr-/-Trem2-/- atherosclerotic mice

Project description:Single-nucleus RNA-seq of aortas was performed in Ldlr-/- and Ldlr-/-Trem2-/- mice fed a high fat diet for 10 weeks

2024-01-12 | GSE243086 | GEO

Bulk RNA-sequencing in Ldlr-/- or Ch25h-/-;Ldlr-/- peritoneal macrophages treated with LPS

Project description:Here we study the effect of LPS in the transcriptome of thioglycollate-elicited peritoneal macrophages isolated from Ldlr knock out and Ch25h;Ldlr double knock out mice

2022-07-01 | GSE189079 | GEO

Liver gene expression profiles of Tribbles-homolog1 (Trib1)/Ldl-receptor (Ldlr) double-knockout mice against Ldlr-knockout mice

Project description:Genetic variants at the TRIB1 (Tribbles-homolog 1) gene locus are strongly associated with plasma lipid traits and the risk of coronary artery disease in humans. In this study, we analyzed the consequences of Trib1-deficiency (Trib1-/-) on hepatic gene expression in mice on the atherosclerosis-susceptible LDL-receptor deficient (Ldlr-/-) background. Therefore, Trib1-/- mice were crossed onto the Ldlr-/- background to generate double knockout mice (Trib1-/-Ldlr-/-) and fed a semisynthetic, modified AIN76 diet (0.02% cholesterol, 4.3% fat). At 20 weeks of age, Trib1-/-Ldlr-/- mice and Trib1+/+Ldlr-/- control mice were sacrificed and liver tissue was snap frozen in liquid nitrogen and stored at -80°C until further processing. Total RNA was isolated from liver tissue (n=8 mice per genotype) and subjected to microarray gene expression analysis.

2023-03-15 | E-MTAB-12669 | biostudies-arrayexpress

The role of LDLR in intestinal inflammation

Project description:Low-density lipoprotein (LDL) is a risk factor for atherosclerosis, obesity, and other metabolic diseases, but its role in colitis is unknown. Here, we investigated the role of LDL in colitis by using LDL receptor deficient mice (Ldlr-/-). Wild-type and Ldlr-/- mice were fed with 3% DSS for 5 days and colons tissues were collected at day 8 post DSS treatment. We observed that Ldlr-/- mice are less susceptible to colitis. To understand the role of LDLR in colitis pathogenesis, we isolated RNA from colons of WT and Ldlr-/- mice and perfoemed RNA-seq. Our data show that the expression of inflamamtory genes are reduced in Ldlr-/- colons compared to wild-type. These data suggest that LDL is a potent endogenous trigger for intestinal inflammation.

2024-11-01 | GSE277062 | GEO

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