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Gene expression for eNOS S1176 mutant mice

ABSTRACT: Gene expression for eNOS S1176 mutant mice

PROVIDER: PRJNA1015707 | ENA |

REPOSITORIES: ENA

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Gene expression for eNOS S1176 mutant mice

Project description:Extensive reports in the past decade have shown the importance of eNOS expression in atherogenesis. However, both the eNOS knockout and overexpression mouse models exhibit paradoxical results of increased atherosclerotic lesions. Our genetic approach herein utilizes endogenous point-mutations at the eNOS S1176 site to effectively manipulate eNOS activity rather than total eNOS protein expression levels. Our efforts definitively show that eNOS S1176 phosphorylation is sufficient to mitigate atherosclerotic lesion progression.

2023-11-10 | GSE243000 | GEO

Transcriptional profiling identifies white matter changes in eNOS+/- mice I

Project description:To elucidate the effects of eNOS deficiency at the transcriptional level, we performed RNA-seq on white matter and grey matter regions dissected from the brains of eNOS+/+ and eNOS+/- mice

2022-07-12 | GSE207961 | GEO

Gene expression profiles of diabetic kidney disease and neuropathy in eNOS knockout mice

Project description:Gene expression profiles of diabetic kidney disease and neuropathy in eNOS knockout mice

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Exercise and transcriptional analysis in male eNOS Knockout Mice

Project description:There is cardiac dysfunction in male eNOS (-/-) with age and 50% mortality at 21M. It was of interest to investigate the gene expression profile of aged eNOS (-/-) male in comparison to (+/+) in order to explore the genetic markers and molecular mechanisms leading to heart failure. RNA was extracted from the left ventricle from male (-/-) (n=3) and (+/+) (n=4) at the age of 21M. Keywords = eNOS knockout Keywords = microarray Keywords = exercise Keywords: other

2005-07-20 | GSE1988 | GEO

The alterations of gene expression in aorta from endothelial nitric oxide synthase (eNOS)-deficient mice

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.

2018-12-15 | GSE123855 | GEO

Transcriptional profiling identifies white matter changes in eNOS+/- mice II

Project description:To elucidate the effects of Sodium nitrate feeding eNOS deficiency at the transcriptional level, RNA-seq was performed on white matter region dissected from the brains of eNOS+/+ and eNOS-/- and eNOS -/- + Sodium Nitrate treatment

2022-07-12 | GSE207960 | GEO

The alterations of gene expression in aorta from endothelial nitric oxide synthase (eNOS)-deficient mice

Project description:The alterations of gene expression in aorta from endothelial nitric oxide synthase (eNOS)-deficient mice

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Gene expression profiles of diabetic kidney disease and neuropathy in eNOS knockout mice: predictors of pathology and RAAS blockade effects

Project description:Diabetic kidney disease (DKD) and diabetic peripheral neuropathy (DPN) are two common diabetic complications. However, their pathogenesis remains elusive and current therapies are only modestly effective. We evaluated genome-wide expression to identify pathways involved in DKD and DPN progression in db/db eNOS -/- mice receiving renin-angiotensin-aldosterone system (RAAS) blocking drugs to mimic the current standard of care for DKD patients. Diabetes and eNOS deletion worsened DKD, which improved with RAAS treatment. Diabetes also induced DPN, which was not affected by eNOS deletion or RAAS blockade. Given the multiple factors affecting DKD and the graded differences in disease severity across mouse groups, an automatic data-analysis method, SOM or self-organizing map was used to elucidate glomerular transcriptional changes associated with DKD, whereas pairwise bioinformatics analysis was used for DPN. These analyses revealed that enhanced gene expression in several pro-inflammatory networks and reduced expression of development genes correlated with worsening DKD. Although RAAS treatment ameliorated the nephropathy phenotype, it did not alter the more abnormal gene expression changes in kidney. Moreover, RAAS exacerbated expression of genes related to inflammation and oxidant generation in peripheral nerves. The graded increase in inflammatory gene expression and decrease in development gene expression with DKD progression underline the potentially important role of these pathways in DKD pathogenesis. Since RAAS blockers worsened this gene expression pattern in both DKD and DPN, it may partly explain the inadequate therapeutic efficacy of such blockers.

2022-07-08 | GSE159059 | GEO

eNOS interactors in human cells

Project description:Endothelial nitric oxide synthase (eNOS) catalyzes the conversion of L-arginine and molecular oxygen into L-citrulline and nitric oxide (NO), a gaseous second messenger that influences cardiovascular physiology and disease. Several mechanisms regulate eNOS activity and function, including phosphorylation at Ser and Thr residues and protein-protein interactions. Combining a tandem affinity purification approach and mass spectrometry, we identified stromal cell-derived factor 2 (SDF2) as a component of the eNOS macromolecular complex in endothelial cells. SDF2 knockdown impaired agonist stimulated NO synthesis and decreased phosphorylation of eNOS at Ser1177, a key event required for maximal activation of eNOS. Conversely, SDF2 overexpression dose-dependently increased NO synthesis through a mechanism involving Akt and calcium (induced with ionomycin), which increased the phosphorylation of Ser1177 in eNOS. NO synthesis by iNOS (inducible NOS) and nNOS (neuronal NOS) was also enhanced upon SDF2 overexpression. We found that SDF2 was a client protein of the chaperone protein Hsp90, interacting preferentially with the M domain of Hsp90, which is the same domain that binds to eNOS. In endothelial cells exposed to vascular endothelial growth factor (VEGF), SDF2 was required for the binding of Hsp90 and calmodulin to eNOS, resulting in eNOS phosphorylation and activation. Thus, our data describe a function for SDF2 as a component of the Hsp90-eNOS complex that is critical for signal transduction in endothelial cells.

2018-10-24 | PXD002598 | Pride

Transcriptional profiling identifies white matter changes in eNOS+/- mice

Project description:Transcriptional profiling identifies white matter changes in eNOS+/- mice

| PRJNA857742 | ENA