Project description:The purpose of this study is to comprehensively elucidate the role of nitric oxide and nitric oxide synthase isoforms in pulmonary emphysema using cap analysis of gene expression (CAGE) sequencing.
Project description:The dysfunction of endothelial nitric oxide synthase may be involved in development of atherosclerosis; however, the underlying molecular and cellular mechanisms of atherosclerosis are poorly understood. Here, we investigated gene expressionsin relation to atherosclerosis using endothelial nitric oxide synthase (eNOS)-deficient mice.
Project description:We describe the effects of restraint stress in presence or absence of an inhibitor of nitric oxide synthase on metastasis formation in lungs of in vivo syngeneic model of mouse breast cancer analysed by whole genome expression microarrays
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.
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
Project description:Aims: Cardiomyocyte-specific nitric oxide synthase 3 (NOS3) overexpression reduces left ventricular (LV) remodelling after myocardial infarction in mice, but its effect on sustained LV pressure-overload remains incompletely understood. We investigated LV structural and functional adaptation to elevated afterload in mice with cardiomyocyte-restricted NOS3 overexpression (NOS3TG) and wild type littermates (WT). Methods and Results: Hemodynamic indices, cardiac hypertrophy and interstitial fibrosis were measured 10 weeks after transverse aortic constriction (TAC). After 10 weeks TAC, NOS3TG had better preserved systolic function (maximum rates of pressure development normalized to maximal pressure 77±6 versus 65±2 ms-1, P=0.05), reduced heart weight-body weight ratio (HW/BW, 5.0±0.3 versus 5.8±0.1, P<0.05), and cardiomyocyte width than WT (14.9±0.4 vs 16.7±0.2 ?m, P<0.05). After 10 weeks TAC, a 44k cDNA chip-based microarray analysis was validated using real time PCR and revealed significantly altered expression pattern of genes involved in cellular growth, matrix remodelling, and inflammation between genotypes. Conclusions: Cardiomyocyte-restricted NOS3 overexpression attenuates TAC-induced hypertrophy via autocrine inhibition of cardiomyocyte cell growth, but does not mitigate myocardial fibrosis. The subsequent diastolic dysfunction suggests that inhibition of matrix producing cells during hypertrophic stress is necessary to prevent functional and structural deterioration of the pressure-overloaded heart. Left ventricular mRNA expression profiles were compared between alpha-myosin heavy chain driven nitric oxide synthase 3 (alpha-MHC-NOS3) transgenic and wild type (WT) littermate mice at baseline and 10 weeks after transversal aortic constrcition-induced pressure-overload. Biological repeats: n=4, two males and two females, for each group and condition. Transgenic mice were backcrossed for seven generations (F7) to a C57Bl/6 N background and age and weight matched animals were used for microarray experiments.
Project description:DNA microarray analysis was employed to investigate the transcriptome response to nitric oxide in Pseudomonas aeruginosa. We focused on the role played by the nitric oxide-response regulators DNR and FhpR and an oxygen-response regulator ANR in the response. The transcriptome profiles of the P. aeruginosa strains before and after exposure to nitric oxide under the microaerobic conditions were analyzed. Wild type, its anr, dnr, and fhpR mutants, and the anr mutant that express dnr were used for the analyses.