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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]

ABSTRACT: 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]

PROVIDER: PRJNA1006685 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25688569.fastq.gz	Fastqsanger.gz
	SRR25688569_1.fastq.gz	Fastqsanger.gz
	SRR25688569_2.fastq.gz	Fastqsanger.gz
	SRR25688570_1.fastq.gz	Fastqsanger.gz
	SRR25688570_2.fastq.gz	Fastqsanger.gz

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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

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:Our study provides the first direct evidence supporting a fibroblast-mediated mechanism of dysfunction and adverse remodeling in the diabetic heart, highlighting the importance of interstitial cells in the pathogenesis of diabetic cardiomyopathy. Diabetes-associated activation of the TGF-b/Smad3 cascade may promote dysfunction not only by accentuating ECM deposition and crosslinking, but also by modulating cardiomyocyte phenotype and function. Thus, the TGF-b system may be a promising therapeutic target in patients with diabetes-associated heart failure.

2024-08-18 | GSE241176 | GEO

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

2011-07-13 | GSE28598 | GEO

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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TGF-beta/Smad3-dependent gene expression analysis in naive CD4 T cells

Project description:Investigation of transcript level modulation in unstimulated and TGF-beta treated (with or without superimposed T-cell receptor and CD28 stimulation) naive CD4 T cells from wild type or Smad3-deficient littermate mice. Smad3 is a critical signaling molecule and transcription factor downstream of TGF-beta and mediates several of the TGF-beta dependent tolerogenic effects in T cells. This study was undertaken to unveil the transcriptionnal program controled by the TGF-b/Smad3 axis. Microarray study using RNA recovered after 6 hours of culture in either serum free media, serum-free media + TGF-beta (2.5ng/ml) or serum-free media + TGF-beta and anti-CD3e and anti-CD28 stimulation (3 conditions). Naive CD4 T cells (TCRb+, CD4+, CD62L+ and CD44-) were sorted from either wild type or Smad3 deficient littermates and submitted to the 3 culture conditions. Three biological replicates were obtained (each from at least 2 different mice). Thus a total of 18 Nimblegen 365K chip were used.

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TGF-Î²/Smad3 Stimulates Stem Cell/Developmental Gene Expression and Vascular Smooth Muscle Cell De-Differentiation

Project description:In order to determine a mechanism through which TGF-b/Smad3 promote these effects, Affymetrix gene expression arrays were performed on primary rat SMCs infected with Smad3 and stimulated with TGF-b or infected with GFP alone. More than 200 genes were differentially expressed (>2.0 fold change, p<0.05) in TGF-b/Smad3 stimulated SMCs. We then performed GO term enrichment analysis using the DAVID bioinformatics database and found that TGF-b/Smad3 activated the expression of multiple genes related to either development or cell differentiation, several of which have been shown to be associated with multipotent stem or progenitor cells. Vascular smooth muscle cells from 3 rats were infected with adenovirus expressing Smad3 and treated with TGF-B for 24 h (TGF-B/Smad3 group). Adenovirus expressing GFP (GFP group) was control. TGF-B/Smad3 treated or control cells were used for RNA extraction and hybridization on Affymetrix microarrays (n=3).

2014-02-04 | E-GEOD-54624 | biostudies-arrayexpress

TGF-beta/Smad3-dependent gene expression analysis in naive CD4 T cells

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TGF-β/Smad3 Stimulates Stem Cell/Developmental Gene Expression and Vascular Smooth Muscle Cell De-Differentiation

2014-02-04 | GSE54624 | GEO

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

| PRJNA1006675 | ENA

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