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Mitochondrial functional aberrations in a mouse model of non-ischemic heart failure

ABSTRACT: We characterized the metabolic and cardiac mitochondrial function in a mouse model of non-ischemic HF. Inhibition of nitric oxide synthesis and hypertension, which often present together, are two important risk factors in human non-ischemic HF. Compared with L-NAME L-NG-Nitroarginine methyl ester (L-NAME), an inhibitor of nitric oxide synthesis or Angiotensin II (AngII), a hypertensive agent treatment alone, L-NAME+AngII induced the most severe HF phenotype characterized by edema, hypertrophy, fibrosis, increased blood pressure and reduced ejection fractions. L-NAME+AngII treated mice had robust deterioration of cardiac mitochondrial function we observed. Microarray analyses revealed majority of the gene changes attributed to the combination of L-NAME+AngII. Pathway analyses indicated significant changes in metabolic pathways such as mitochondrial oxidative phosphorylation, fatty acid metabolism and tricarboxylic acid pathways etc.in L-NAME+AngII hearts. We conclude that combination of L-NAME+AngII exacerbates cardiac contractile and mitochondrial functional de-regulation compared with L-NAME and AngII alone, resulting in non-ischemic HF. This model of heart failure may be highly valuable in studying mechanisms and treatments for non-ischemic heart failure.

ORGANISM(S): Mus musculus

PROVIDER: GSE72132 | GEO | 2016/01/19

SECONDARY ACCESSION(S): PRJNA293126

REPOSITORIES: GEO

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Mitochondrial functional aberrations in a mouse model of non-ischemic heart failure

Project description:We characterized the metabolic and cardiac mitochondrial function in a mouse model of non-ischemic HF. Inhibition of nitric oxide synthesis and hypertension, which often present together, are two important risk factors in human non-ischemic HF. Compared with L-NAME L-NG-Nitroarginine methyl ester (L-NAME), an inhibitor of nitric oxide synthesis or Angiotensin II (AngII), a hypertensive agent treatment alone, L-NAME+AngII induced the most severe HF phenotype characterized by edema, hypertrophy, fibrosis, increased blood pressure and reduced ejection fractions. L-NAME+AngII treated mice had robust deterioration of cardiac mitochondrial function we observed. Microarray analyses revealed majority of the gene changes attributed to the combination of L-NAME+AngII. Pathway analyses indicated significant changes in metabolic pathways such as mitochondrial oxidative phosphorylation, fatty acid metabolism and tricarboxylic acid pathways etc.in L-NAME+AngII hearts. We conclude that combination of L-NAME+AngII exacerbates cardiac contractile and mitochondrial functional de-regulation compared with L-NAME and AngII alone, resulting in non-ischemic HF. This model of heart failure may be highly valuable in studying mechanisms and treatments for non-ischemic heart failure. Twelve week-old C57BL6 male mice were randomly assigned to 4 groups: 1. Control, 2. L-NAME treatment, 3. AngII treatment, 4. L-NAME+AngII treatment.L-NAME (0.3 mg/ml with 1% NaCl) was administered in drinking water. AngII (0.7 mg/kg/day) was administered via subcutaneous micro-osmotic pumps. L-NAME and AngII were administered to mice for 5 weeks and 4 weeks in combination to induce HF or alone to study the effects of the individual agents.

2016-01-19 | E-GEOD-72132 | biostudies-arrayexpress

Real-time quantitative PCR analysis of long non-codign RNAs transcripts in non-end stage heart failure patients

Project description:Left ventricle (LV) cardiac biopsies from patients affected by non-end-stage dilated hypokinetic ischemic cardiomyopathy (HF) where collected during Surgical Ventricular Restoration procedure.

2016-07-11 | GSE77399 | GEO

Transcription profiling of Cd-induced nitric oxide synthesis in Arabidopsis

Project description:Cadmium treatment induces slow but long lasting nitric oxide production in plant tissues. This NO production can be suppressed using the commonly used Nitric Oxide Synthase inhibitor L-NAME. This inhibitor tends to partially alleviate Cd toxicity. This effect is correlated with a strong diminution of Cd content in roots of plants treated both with Cd and L-NAME compared to roots from plants treated with Cd only. The main goal of this study is the identification of transcriptionnal changes caused by Cd-induced nitric oxide, and that could potentially result in enhanced Cd root accumulation.

2007-12-08 | E-MEXP-508 | biostudies-arrayexpress

Artemisinin mimics calorie restriction to trigger mitochondrial biogenesis and compromise telomere shortening in mice

Project description:Calorie restriction is known to extend lifespan among organisms by a debating mechanism underlying nitric oxide-driven mitochondrial biogenesis. We report here that nitric oxide generators including artemisinin, sodium nitroprusside, and L-arginine mimics calorie restriction and resembles hydrogen peroxide to initiate the nitric oxide signaling cascades and to elicit the global antioxidative responses in mice. The large quantities of antioxidant enzymes are correlated with the low levels of reactive oxygen species, which allow the down-regulation of tumor suppressors and accessory DNA repair partners, eventually leading to the compromise of telomere shortening. Accompanying with the up-regulation of kinases, acetylases, and biomarkers, mitochondrial biogenesis occurs with the elevation of adenosine triphosphate levels upon exposure of mouse skeletal muscles to the mimetics of calorie restriction. In conclusion, calorie restriction-triggered nitric oxide provides antioxidative protection and alleviates telomere attrition via mitochondrial biogenesis, thereby maintaining chromosomal stability and integrity, which are the hallmarks of longevity. Six samples were analyzed, in which a control sample was included.

2015-02-18 | E-GEOD-65993 | biostudies-arrayexpress

Proteomic assessment of C57BL/6 hippocampi after non-selective pharmacological inhibition of all nitric oxide synthase activity

Project description:Nitric oxide is the smallest gaseous signaling molecule responsible for maintaining homeostasis in a myriad of tissues and molecular pathways in neurological and cardiovascular pathologies. In recent years, there has been increasing interest in the potential interaction between arterial stiffness (AS), an independent cardiovascular risk factor, and neurodegenerative syndromes given increasingly epidemiological study reports. For this reason, we previously sought to investigate the mechanistic convergence between AS and neurodegeneration via the progressive non-selective inhibition of all nitric oxide synthase (NOS) isoforms with N(G)-nitro-L-arginine methyl ester (L-NAME) in C57BL/6 mice. Our results showed progressively increased arterial stiffness in vivo and impaired visuospatial learning and memory in L-NAME treated C57BL/6 mice. In this study, we sought to further investigate the progressive molecular signatures in hippocampal tissue via LC-MS/MS proteomic analysis

2022-08-12 | PXD033646 | Pride

Artemisinin mimics calorie restriction to trigger mitochondrial biogenesis and compromise telomere shortening in mice

2015-02-18 | GSE65993 | GEO

Transcriptome analysis of diabetic and non diabetic patients affected by post-ischemic heart failure

Project description:Increased morbidity and mortality associated with post-ischemic heart failure (HF) in diabetic patients underscore the need for a better understanding of the underlying molecular events. Indeed, effective HF therapy in diabetic patients requires a complex strategy encompassing the development of improved diagnostic and prognostic markers and innovative pharmacological approaches. Whole mRNAs expression was measured in the heart of patients with heart failure (HF) with or without concomitant Type 2 diabetes mellitus (T2DM) and compared it to control non-failing hearts. We identified distinct genes modulated in HF patients compared to controls, as well as to T2DM HF patients compared to not diabetic HF patients. Our study included left ventricle (LV) cardiac biopsies taken from the vital, non-infarcted zone (remote zone) derived from patients affected by dilated hypokinetic post-ischemic cardiomyopathy, undergoing surgical ventricular restoration procedure. Inclusion criteria for diabetic were: GLICEMIA: >=126 mg/dl, previous T2DM diagnosis or anti-diabetic therapy, while for non diabetic: GLICEMIA: <100 mg/dl and HbA1c: n.v. 4.8-6.0%. Moreover, HF patients were matched for End Systolic Volume (ESV), Ejection fraction (LVEF), Age, Sex, Ethnic distribution, Smoke habits, Hypertension, Glomerular filtration rate (GFR), Body Mass Index (BMI). Genes expression was assessed by Affymetrix GeneChips Human Gene 1.0 ST array, using total RNA extracted from 7 T2DM HF patients, 12 non-T2DM HF patients and 5 controls.

2012-03-21 | E-GEOD-26887 | biostudies-arrayexpress

No-Transcriptional impact of Cd-induced nitric oxide synthesis

Project description:rs05-08_no - no - Cadmium treatment induces slow but long lasting nitric oxide production in plant tissues. This NO production can be suppressed using the commonly used Nitric Oxide Synthase inhibitor L-NAME. This inhibitor tends to partially alleviate Cd toxicity. This effect is correlated with a strong diminution of Cd content in roots of plants treated both with Cd and L-NAME compared to roots from plants treated with Cd only. The main goal of this study is the identification of transcriptionnal changes caused by Cd-induced nitric oxide, and that could potentially result in enhanced Cd root accumulation. - Germination of surface sterilized seeds was performed on solid MS/2 medium. After 2 weeks, the young plantlets were placed on sand for an additional 3 week period in a controlled environment (8 h photoperiod of 300 umol m-2 s-1, 22degreeC, 70% relative humidity) . Plants of similar rosette diameters were then transfered to an hydroponic culture using the nutritive solution described in [Gravot et al. 2004 FEBS Letters 561:22-28] for an acclimation of 3 days. L-NAME and cadmium treatments were respectively started 1 and 2 hours after the start of illumination and root tissues were collected 24 h later and immediatly frozen in liquid nitrogen before RNA extraction. Treatments were : 1 : control 2 : L-NAME 5 mM 3 : Cd 30 uM 4 : L-NAME 5mM + Cd 30 uM 5 : Cd 15 uM For each condition, 3 independent biological repetitions were conducted. RNA were extracted separatly and checked for quality before pooling together. Keywords: treated vs untreated comparison

2007-05-31 | GSE7945 | GEO

AngII induced responses from non-myocytes in the heart

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2022-02-08 | GSE185756 | GEO

Oleic acid-dependent modulation of Nitric Oxide Associated 1 protein levels regulate nitric oxide mediate signaling in plant defense.

Project description:Oleic acid-dependent modulation of Nitric Oxide Associated 1 protein levels regulate nitric oxide- mediate signaling in plant defense. Nitric Oxide, Oleic acid, Salicylic acid, Arabidopsis, Defense

2012-08-01 | GSE36797 | GEO

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