E-PROT-92
Ontology highlight
ABSTRACT:
PROVIDER: E-PROT-92 | ExpressionAtlas | 2022-01-10
REPOSITORIES: ExpressionAtlas
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Project description:Cardiac proteome analysis of obese rats treated with mitoQ
2023-06-29 | PXD034955 | JPOST Repository
Project description:Aims: Despite the high prevalence of heart failure with preserved ejection fraction (HFpEF), the pathomechanisms remain elusive and specific therapy is lacking. Disease-causing factors include metabolic risk, notably obesity. However, proteomic changes in HFpEF are poorly understood, hampering therapeutic strategies. We sought to elucidate how metabolic syndrome affects cardiac protein expression, phosphorylation and acetylation in the Zucker diabetic fatty/Spontaneously hypertensive heart failure F1 (ZSF1) rat HFpEF model, and to evaluate some changes regarding their potential for treatment. Main methods: ZSF1 obese and lean rats were fed a Purina diet up to the onset of HFpEF in the obese animals. We quantified the proteome, phosphoproteome and acetylome of ZSF1 obese versus lean heart tissues by mass spectrometry and singled out targets for site-specific evaluation. Key findings: We found the acetylome of ZSF1 obese versus lean hearts more severely altered (21% of proteins changed) than the phosphoproteome (9%) or proteome (3%). Proteomic alterations, confirmed by immunoblotting, indicated low-grade systemic inflammation and endothelial remodeling in obese hearts, but low nitric oxide-dependent oxidative/nitrosative stress. Altered acetylation in ZSF1 obese hearts mainly affected pathways important for metabolism, energy production and mechanical function, including hypo-acetylation of mechanical proteins but hyper-acetylation of proteins regulating fatty acid metabolism. Hypo-acetylation and hypo-phosphorylation of elastic titin in ZSF1 obese hearts explained myocardial stiffening. Significance: Cardiometabolic syndrome alters posttranslational modifications, notably acetylation, in experimental HFpEF. Pathway changes implicate a HFpEF signature of low-grade inflammation, endothelial dysfunction, metabolic and mechanical impairment, and suggest titin stiffness and mitochondrial metabolism as promising therapeutic targets.
2022-10-12 | PXD036259 | Pride
Project description:Obesity is a complex metabolic disease considered a global pandemic and associated with high incidence of cardiovascular disease. The excess of adipose tissue may promotes maladaptation that result in alterations in structure and function of the heart; however, the mechanisms are not fully elucidated. Proteomics may provide a deeper understanding into the pathophysiological process and contribute to the identification of new potential therapeutic targets. Thus, the aim of this was evaluate the myocardial protein expression in healthy and obese rats induced by Western diet to better comprehend the network of mechanisms inherent to cardiac dysfunction in obesity. For this purpose, we performed proteomic approaches based on nano-liquid chromatography-tandem mass spectrometry (nLC-MS/MS) followed by label-free quantification.
2019-12-04 | PXD013543 | Pride
Project description:The effects of exercise training (ET) on the heart of aortic stenosis (AS) rats are controversial and the mechanisms involved in alterations induced by ET have been poorly clarified. In this study we analyzed the myocardial proteome to identify proteins modulated by moderate intensity aerobic ET in rats with chronic supravalvar AS. Wistar rats were divided into four groups: sedentary control (C-Sed), exercised control (C-Ex), sedentary aortic stenosis (AS-Sed), and exercised AS (AS-Ex). ET consisted of five treadmill running sessions per week for 16 weeks. Statistical analysis was performed by ANOVA or Kruskal-Wallis and Goodman tests. Results were discussed at a significance level of 5%. At the end of the experiment, AS-Ex rats had higher functional capacity, lower blood lactate concentration, and better cardiac structural and left ventricular functional parameters than the AS-Sed. Myocardial proteome analysis showed that AS-Sed had higher protein expressions related to the glycolytic pathway, oxidative stress, and inflammation, and lower protein expressions related to beta-oxidation than C-Sed. AS-Ex had higher expression of one protein related to mitochondrial biogenesis and lower protein expressions associated with oxidative stress and inflammation than AS-Sed. Proteomic data were validated for proteins related to lipid and glycolytic metabolism. In conclusion, chronic pressure overload changes the expression of myocardial proteins that are mainly involved in lipid and glycolytic energy metabolism in rats. Moderate intensity aerobic training attenuates protein expressions related to oxidative stress and inflammation and increases protein expressions related to mitochondrial biogenesis. Protein changes are associated with improved functional capacity, cardiac remodeling and left ventricular function in aortic stenosis rats.
2024-02-29 | PXD040785 | Pride
Project description:Angiotensin-(1-7) (Ang-(1-7)) is an endogenous heptapeptide from the renin-angiotensin system. The cardioprotective role of Ang-(1-7) has been described due to its anti-inflammatory and anti-fibrotic activities. In this context, we investigated the impact of the oral formulation of Ang-(1-7) vehiculized in hydroxypropyl β-cyclodextrin (HPβCD) on cardiac proteome remodeling after experimental myocardial infarction. For this, Wistar male rats were submitted to short- (7 days) or long-term (60 days) oral treatment with HPβCD/Ang-(1-7) after induction of experimental myocardial infarction (MI)
2019-08-19 | PXD012896 | Pride
Project description:Heart failure with preserved ejection fraction (HFpEF) is a highly prevalent and intractable form of cardiac decompensation commonly associated with diastolic dysfunction. Here, we show that diastolic dysfunction in patients with HFpEF is associated with a cardiac deficit in nicotinamide adenine dinucleotide (NAD+). Elevating NAD+ by oral supplementation of its precursor, nicotinamide, improved diastolic dysfunction induced by aging (in 2-year-old C57BL/6J mice), hypertension (in Dahl salt-sensitive rats) or cardiometabolic syndrome (in ZSF1 obese rats). Mechanistically, this effect was mediated partly through alleviated systemic comorbidities and enhanced myocardial bioenergetics, as evidenced by cardiac trasncriptome and metabolome analyses. Simultaneously, nicotinamide directly improved cardiomyocyte passive stiffness and calcium-dependent active relaxation through increased deacetylation of titin and the sarcoplasmic reticulum calcium ATPase 2a, respectively. In a long-term human cohort study, high dietary intake of naturally occurring NAD+ precursors was associated with lower blood pressure and reduced risk of cardiac mortality. Collectively, these results suggest NAD+ precursors, and especially nicotinamide, as potential therapeutic agents to treat diastolic dysfunction and HFpEF in humans.
2021-02-11 | GSE163665 | GEO
Project description:Rosiglitazone, a peroxisome proliferator-activated receptor g (PPARg) agonist of the thiazolidinedione class, is a major insulin-sensitizing drug widely used to treat type-2 diabetes. Rosiglitazone causes myocardial hypertrophy in rodents and increases the risk of cardiac events in man. To better characterize its cardiac effects, male Wistar rats were orally administered 0, 10 or 80 mg/kg/day rosiglitazone. Male Wistar rats were orally administered 0, 10 or 80 mg/kg/day rosiglitazone once per day for 14 days. Samples were obtained 6, 24, 168 or 336 hours after the final treatment.
2010-07-29 | E-GEOD-22553 | biostudies-arrayexpress
Project description:This study found that IPC-induced serum exosomes inhibit myocardial fibrosis and improve cardiac function following MI by transferring miR-133a-3p, which targets LTBP1 and PPP2CA, to regulate the TGF-β signaling pathway in rats.
2024-09-18 | GSE272122 | GEO
Project description:Thyroid hormone improves left ventricular remodeling and cardiac performance after myocardial infarction (MI), but the molecular basis is unknown. This study was designed to detect gene expression changes in left ventricular non-infarcted areas at 4 weeks following myocardial infarction with and without thyroid hormone treatment. The results suggest that altered expression of genes for molecular function and biological process may be involved in the beneficial effects of thyroid hormone treatment following myocardial infarction in rats. MI was produced by ligation of the left anterior descending coronary artery in female SD rats. Rats were divided into the following groups: (1) Sham MI, (2) MI, and (3) MI+T4 treatment (T4 pellet 3.3mg, 60 days release, implanted subcutaneously immediately following MI). Four weeks after surgery, total RNA was isolated from left ventricular non-infarcted areas for microarray analysis using the Illumina RatRef-12 Expression BeadChip Platform.
2012-04-30 | E-GEOD-35088 | biostudies-arrayexpress