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Endothelial Overexpression protects Metabolic Homeostasis and the Development of Obesity and cardiovascular disease

ABSTRACT: Endothelial Overexpression protects Metabolic Homeostasis and the Development of Obesity and cardiovascular disease

PROVIDER: PRJNA1111579 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29025435_1.fastq.gz	Fastqsanger.gz
	SRR29025435_2.fastq.gz	Fastqsanger.gz
	SRR29025436_1.fastq.gz	Fastqsanger.gz
	SRR29025436_2.fastq.gz	Fastqsanger.gz
	SRR29025437_1.fastq.gz	Fastqsanger.gz

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Endothelial Overexpression protects Metabolic Homeostasis and the Development of Obesity and cardiovascular disease

Project description:Introduction: Obesity is a major risk factor associated with multiple pathological conditions including diabetes and cardiovascular disease. Endothelial dysfunction is an early predictor of obesity. However, little is known regarding how early endothelial changes trigger obesity. In the present work we report a novel endothelial-mediated mechanism essential for regulation of metabolic homeostasis, driven by c-Myc. Methods: We used conditional overexpression (EC-Myc OE) mouse models to investigate the role of endothelial-specific c-Myc in metabolic homeostasis during high-fat diet exposure. Body weight, metabolic parameters and cardiovascular function were collected over time and tissue samples collected at endpoint for biochemical, pathology and RNA-sequencing analysis. Results: In the present study we demonstrate that Overexpression of endothelial c-Myc attenuated diet-induced obesity and visceral fat accumulation and prevented the development of glucose tolerance and cardiac dysfunction. Transcriptome analysis of skeletal muscle suggests that the protective effects promoted by endothelial c-Myc overexpression are associated with the expression of genes known to increase weight loss, energy expenditure and glucose tolerance. Discussion: Our results show a novel important role for endothelial c-Myc in regulating metabolic homeostasis and suggests its potential targeting in preventing obesity and associated complications such as diabetes type-2 and cardiovascular dysfunction.

2024-05-31 | GSE267493 | GEO

Deletion of intestinal Hdac3 remodels the lipidome of enterocytes and protects mice from diet-induced obesity

Project description:Deletion of intestinal Hdac3 remodels the lipidome of enterocytes and protects mice from diet-induced obesity

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Cooperative ETS Transcription Factors Enforce Adult Endothelial Cell Fate and Cardiovascular Homeostasis

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KDM4B epigenetically protects against obesity and metabolic dysfunction

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Protection from obesity and diabetes by blockade of TGF-beta/Smad3 signaling

Project description:Imbalances in glucose and energy homeostasis are at the core of the worldwide epidemic of obesity and diabetes. Here, we illustrate an important role of the TGF-beta/Smad3 signaling pathway in regulating glucose and energy homeostasis. Smad3 deficient mice are protected from diet-induced obesity and diabetes. Interestingly, the metabolic protection is accompanied by Smad3-/- white adipose tissue acquiring the bioenergetic and gene expression profile of brown fat/skeletal muscle. Smad3-/- adipocytes demonstrate a marked increase in mitochondrial biogenesis, with a corresponding increase in basal respiration, and Smad3 acts as a repressor of PGC-alpha1 expression. We observe significant correlation between TGF-beta1 levels and adiposity in rodents and humans. Further, systemic blockade of TGF-beta1 signaling protects mice from obesity, diabetes and hepatic steatosis. Together, these results demonstrate that TGF-beta signaling regulates glucose tolerance and energy homeostasis and suggest that modulation of TGF-beta1 activity might be an effective treatment strategy for obesity and diabetes. Smad3-/- and WT mice were fed with regular diet (RD) and high fat diet (HFD), and diet induced obese (DIO) mice were treated with IgG and anti-TGF-b1 antibody

2011-07-12 | E-GEOD-28598 | biostudies-arrayexpress

Cooperative ETS Transcription Factors Enforce Adult Endothelial Cell Fate and Cardiovascular Homeostasis [Liver_IL1B_TNFA_RNAseq]

Project description:Cooperative ETS Transcription Factors Enforce Adult Endothelial Cell Fate and Cardiovascular Homeostasis [Liver_IL1B_TNFA_RNAseq]

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Cooperative ETS Transcription Factors Enforce Adult Endothelial Cell Fate and Cardiovascular Homeostasis [ECs_InVivo_D10_RNAseq]

Project description:Cooperative ETS Transcription Factors Enforce Adult Endothelial Cell Fate and Cardiovascular Homeostasis [ECs_InVivo_D10_RNAseq]

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Cooperative ETS Transcription Factors Enforce Adult Endothelial Cell Fate and Cardiovascular Homeostasis [Liver_InVivo_ATACseq]

Project description:Cooperative ETS Transcription Factors Enforce Adult Endothelial Cell Fate and Cardiovascular Homeostasis [Liver_InVivo_ATACseq]

| PRJNA891050 | ENA

Cooperative ETS Transcription Factors Enforce Adult Endothelial Cell Fate and Cardiovascular Homeostasis [Brain_InVitro_RNAseq]

Project description:Cooperative ETS Transcription Factors Enforce Adult Endothelial Cell Fate and Cardiovascular Homeostasis [Brain_InVitro_RNAseq]

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Cooperative ETS Transcription Factors Enforce Adult Endothelial Cell Fate and Cardiovascular Homeostasis II

Project description:Cooperative ETS Transcription Factors Enforce Adult Endothelial Cell Fate and Cardiovascular Homeostasis II

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