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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]

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE241177 | GEO | 2024/08/18

REPOSITORIES: GEO

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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]

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.

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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]

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Transcription profiling of rat ventricle samples from streptozotocin (STZ)-diabetic animals to investigate mitochondrial long-chain free fatty acid export

Project description:Cardiomyopathy in type 1 diabetic patients is characterized by early onset diastolic and late onset systolic dysfunction. The mechanism underlying development of diastolic and systolic dysfunction in diabetes remains unknown. We used microarrays to detail the ventricle gene expression changes that underly development of diabetic cardiomyopathy. We identified distinct classes of up-regulated genes during this process. Experiment Overall Design: 150g male Wistar rats (Harlan) we injected with 65 mg/kg streptozotocin to induce Type 1 diabetes. Four replicates of Control and Diabetic rat ventricles were removed and frozen at Three time points for total RNA isolation and hybridization on the Affymetrix RG-U34A microarray. The 3 day samples show a baseline for initial diabetic changes in the ventricle. The 28 day samples show changes associated with diastolic dysfunction in diabetes. The 42 day samples show changes associated with both diastolic and systolic dysfunction in type 1 diabetic rat ventricles.

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Expression data from Rat ventricles 3 days/28 days/42 days after STZ injection

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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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Ago2 protects against diabetic cardiomyopathy via activating mitochondrial gene translation [Ribosome-seq]

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Ago2 protects against diabetic cardiomyopathy via activating mitochondrial gene translation [mRNA-seq]

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Ago2 protects against diabetic cardiomyopathy via activating mitochondrial gene translation [Ribo-seq]

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Ago2 protects against diabetic cardiomyopathy via activating mitochondrial gene translation II

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