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Fibroblast-specific TGF-b signaling mediates dysfunction, fibrosis and hypertrophy in a mouse model of obesity-associated type 2 diabetes [RNA-seq: TSP4 OE]

ABSTRACT: Fibroblast-specific TGF-b signaling mediates dysfunction, fibrosis and hypertrophy in a mouse model of obesity-associated type 2 diabetes [RNA-seq: TSP4 OE]

PROVIDER: PRJNA1006688 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25688581_1.fastq.gz	Fastqsanger.gz
	SRR25688581_2.fastq.gz	Fastqsanger.gz
	SRR25688582_1.fastq.gz	Fastqsanger.gz
	SRR25688582_2.fastq.gz	Fastqsanger.gz
	SRR25688583_1.fastq.gz	Fastqsanger.gz

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Fibroblast-specific TGF-b signaling mediates dysfunction, fibrosis and hypertrophy in a mouse model of obesity-associated type 2 diabetes [RNA-seq: TSP4 OE]

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Fibroblast-specific TGF-b signaling mediates dysfunction, fibrosis and hypertrophy in a mouse model of obesity-associated type 2 diabetes [RNA-seq: TSP4 stimulation]

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Fibroblast-specific TGF-b signaling mediates dysfunction, fibrosis and hypertrophy in a mouse model of obesity-associated type 2 diabetes

Project description:Fibroblast-specific TGF-b signaling mediates dysfunction, fibrosis and hypertrophy in a mouse model of obesity-associated type 2 diabetes

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Fibroblast-specific TGF-b signaling mediates dysfunction, fibrosis and hypertrophy in a mouse model of obesity-associated type 2 diabetes

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Fibroblast-specific TGF-b signaling mediates dysfunction, fibrosis and hypertrophy in a mouse model of obesity-associated type 2 diabetes [RNA-seq: TSP4 stimulation]

Project description:Fibroblast-specific TGF-b signaling mediates dysfunction, fibrosis and hypertrophy in a mouse model of obesity-associated type 2 diabetes [RNA-seq: TSP4 stimulation]

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Fibroblast-specific TGF-b signaling mediates dysfunction, fibrosis and hypertrophy in a mouse model of obesity-associated type 2 diabetes [RNA-seq: Smad3 in dbdb]

Project description:Fibroblast-specific TGF-b signaling mediates dysfunction, fibrosis and hypertrophy in a mouse model of obesity-associated type 2 diabetes [RNA-seq: Smad3 in dbdb]

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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

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