Functional promoter analysis of the endothelial constitutive nitric oxide synthase gene.

by Hariclia Antoniou

Publisher: National Library of Canada in Ottawa

Written in English
Published: Downloads: 233
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Edition Notes

Thesis (M.Sc.) -- University of Toronto, 1995.

SeriesCanadian theses = -- Thèses canadiennes
The Physical Object
Pagination1 microfiche : negative. --
ID Numbers
Open LibraryOL17893873M
ISBN 100612076237

Objective: To examine the effects of two polymorphisms of the endothelial constitutive nitric oxide synthase (ecNOS) gene, 4a/4b(A:B) located in intron 4 and GluAsp(G:T) located in exon 7, on the development of acute coronary syndromes (ACS). Methods: patients with ACS and control participants were investigated for genotype and conventional risk factors. Results. Interleukin-1β–inducible inducible nitric oxide synthase expression and nitric oxide production in aortic endothelial cells. To examine whether IL-1β stimulates NO production, RAECs were stimulated with 10 ng/mL IL-1β and the time course of NO accumulation in the culture medium was determined (Fig. 1A).IL-1β stimulated a robust increase in NO production. Time for primary review 32 days. 1 Introduction. Three different genes encoding endothelial, neuronal, and macrophage nitric oxide synthase have been cloned, illustrating that diverse processes such as vascular signaling, neurotransmission in the brain and cell-mediated toxicity are dependent on the production of nitric oxide. In the cardiovascular system, nitric oxide is a potent.   Endothelial nitric oxide synthase (eNOS) is activated by phosphorylation of serine by the protein kinase Akt/PKB. Since hyperglycemia-induced mitochondrial superoxide overproduction increases O-linked N-acetylglucosamine modification and decreases O-linked phosphorylation of the transcription factor Sp1, the effect of hyperglycemia and the hexosamine .

Balligand JL, Kobzik L, Han X, et al. Nitric oxide-dependent parasympathetic signaling is due to activation of constitutive endothelial (type III) nitric oxide synthase in cardiac myocytes. J Biol Chem. ; – Structure and chromosomal localization of the human constitutive endothelial nitric oxide synthase gene. J Biol Chem –, PubMed ISI Google Scholar; Metzger IF, Sertório JT, Tanus-Santos JE. Modulation of nitric oxide formation by endothelial nitric oxide synthase gene haplotypes. Free Radic Biol Med –,   Nitric oxide synthase, endothelial (EC: Gene expression databases. Bgee i: ENSG, Expressed in spleen and other tissues ExpressionAtlas i: P, baseline and differential: Genevisible i: P, HS: Organism-specific databases Calmodulin-binding Sequence analysis Add BLAST: Nitric oxide (NO), synthesized from l-arginine by NO synthases (NOS), plays an essential role in the regulation of cerebrovascular tone. Adenoviral vectors have been widely used to transfer recombinant genes to different vascular beds. To determine whether the recombinant endothelial NOS (eNOS) gene can be delivered in vivo to the adventitia of cerebral arteries and functionally expressed, a.

Proinflammatory cytokines downregulate gene expression and activity of constitutive nitric oxide synthase in porcine pulmonary artery endothelial cells. Res Commun Mol Pathol Pharmacol ; . The vascular endothelium is a monolayer of cells between the vessel lumen and the vascular smooth muscle cells. Far from being inert, it is metabolically active and produces a variety of vasoactive mediators. Among these mediators, endothelial derived nitric oxide is essential in the maintenance of vascular homeostasis, and defects in the L-arginine: nitric oxide pathway have been implicated.   qPCR analysis of the expression levels of (A) nitric oxide synthase (NOS) and (B) nitrophorin 2 (NP2) genes in the salivary glands of the us . Angiology; INTRODUCTION: Endothelial dysfunction is recognized as an early and initiating event in the pathogenesis of coronary artery disease. Gene polymorphisms of endothelial constitutive nitric oxide synthase (ecNOS), angiotensin converting enzyme (ACE) and angiotensin II type 1 receptor (AT1R) have been found to be associated with atherosclerosis.

Functional promoter analysis of the endothelial constitutive nitric oxide synthase gene. by Hariclia Antoniou Download PDF EPUB FB2

The nitric oxide synthase-3 (NOS3) gene encodes for nitric oxide (NO) synthase, which is responsible for the conversion of L-arginine to NO, a primary vasodilator and regulator of blood flow and vascular tone. 10 – 12 The endothelin-1 (EDN) gene encodes for endothelin-1 (ET-1), a primary vasoconstrictor of vascular smooth muscle by:   Core tip: The present study reveals first molecular epidemiological evidence from south Indian cohort for the association of endothelial nitric oxide synthase T > C promoter polymorphism with a risk to develop gastric cancer (GC).

The CC genotype and C allele of the T > C polymorphism were significantly associated with an elevated risk to GC, probably due to the lowered nitric oxide Cited by: 2. Purchase Nitric Oxide Synthase: Characterization and Functional Analysis, Volume 31 - 1st Edition.

Print Book & E-Book. ISBNPrice: $ Background. Numerous individually underpowered association studies have been conducted on endothelial nitric oxide synthase (eNOS) genetic variants across different ethnic populations, however, the results are often therefore aimed to meta-analyze three eNOS widely-evaluated polymorphisms, GT (rs) in exon 7, 4b/a in intron 4, and T−C (rs) in promoter Cited by:   Introduction.

Nitric oxide (NO) is generated by conversion of L-arginine into L-citrulline and, in platelets, it seems to be predominantly produced by the activity of a constitutive NO synthase 3 (NOS3), although small amounts of an inducible NOS (NOS2) isoform have also been detected.Platelet-derived NO acts as negative feedback mechanisms reducing the recruitment of new platelets Cited by: 9.

Background and Purpose—Nitric oxide (NO) synthesized by endothelial constitutive NO synthase (ecNOS) plays a key role in vascular regulation and is known concerning the role of the ecNOS gene (NOS3) as a risk factor for brain infarction (BI).Our aim was to investigate the relation between the GluAsp polymorphism in exon 7 of NOS3 with BI and its subtypes.

Functional analysis of the human endothelial nitric oxide synthase promoter. J Biol Chem. ; – Crossref Medline Google Scholar; 26 Rasband W.

NIH Image program, v Bethesda, Md: National Institutes of Health; Google Scholar; 27 Van Vliet AK, Negre-Aminou P, van Thiel GC, Bolhuis PA, Cohen LH.

Action of lovastatin. William C. Sessa, in Methods in Neurosciences, Introduction. Endothelial nitric oxide synthase (eNOS) is expressed in a variety of cell types inclusive of endothelial cells, hippocampal neurons, cardiac myocytes, and epithelial cells.

Although once considered a constitutive “housekeeping gene,” evidence suggests that expression of the eNOS gene may be activated via transcriptional.

Nakayama M, Yasue H, Yoshimura M, et al. T −T →C mutation in the 5′-flanking region of the endothelial nitric oxide synthase gene is associated with coronary spasm. Circulation. ; – Niu W, Qi Y. An updated meta-analysis of endothelial nitric oxide synthase gene: three well-characterized polymorphisms with hypertension.

The promoter region of the endothelial constitutive nitric oxide synthase (ecNOS) gene contains a transcriptional factor AP-1 binding element. In the present study, we sought to determine the effect of PKC inhibition on the expression of ecNOS in cultured bovine aortic endothelial cells (BAEC).

Nitric oxide synthases (EC ) (NOSs) are a family of enzymes catalyzing the production of nitric oxide (NO) from is an important cellular signaling molecule. It helps modulate vascular tone, insulin secretion, airway tone, and peristalsis, and is involved in angiogenesis and neural development.

It may function as a retrograde neurotransmitter. Minc-Golomb and J.P. Schwartz, Expression of Constitutive Brain Nitric Oxide Synthase and Inducible Nitric Oxide Synthase by Cultured Neurons and Glia.

A.H. Cheung and P.A. Marsden, Structural Characterization of Human Neuronal Nitric Oxide Synthase Gene: Complex Transcription Unit. W.C. Sessa, Transcriptional Control of Endothelial Nitric.

A smoking-dependent risk of coronary artery disease associated with a polymorphism of the endothelial nitric oxide synthase gene. Nat Med. ; 2: 41– Crossref Medline Google Scholar; 20 Wang XL, Wang J. Endothelial nitric oxide synthase gene sequence variations and vascular disease.

Mol Genet Metab. ; – Nitric oxide (NO) synthesized by endothelial nitric oxide synthase (eNOS) is a key mediator of endothelial function.

We determined the role of 3 potentially functional eNOS polymorphisms (TC, intron 4ab, GT) located toward the 5′ flanking end of the gene as risk factors for SVD and different SVD subtypes: isolated lacunar infarction (n.

Frank M. Faraci, in Methods in Neurosciences, Inducible Nitric Oxide Synthase. Inducible NO synthase is a gene product which, in contrast to endothelial and neuronal isoforms, is not expressed under basal conditions in most cells (4).Expression of inducible NO synthase may occur in response to proinflammatory factors such as lipopolysaccharide and certain cytokines (3, 4).

A meta-analysis of endothelial nitric oxide synthase gene TC polymorphism as a risk factor for acute chest syndrome in sickle cell disease February Meta Gene Nitric Oxide Synthase: Characterization and Functional Analysis.

Edited by Mahin D. Maines. select article [15] - Expression of Constitutive Brain Nitric Oxide Synthase and Inducible Nitric Oxide Synthase by Cultured Neurons and Glia select article [17] - Transcriptional Control of Endothelial Nitric Oxide Synthase Gene Expression.

Haplotype analysis of the endothelial nitric oxide synthase gene in asthma at nucleotide (TC) in the 5′-flanking region of the NOS3 gene results in a significant reduction in eNOS gene promoter activity M. Gharnaout, S.S. Salah, W. Boukouaci, et tutive nitric oxide synthase gene polymorphisms and house dust mite.

Functional Analysis of the Human Endothelial Nitric Oxide Synthase Promoter To gain insights into the mechanisms of endothelial nitric oxide synthase (eNOS) gene expression, we have cloned the eNOS promoter and fused it to a luciferase reporter gene to map regions of the promoter important for basal transcription in bovine aortic.

Abstract Background: Nitric oxide (NO) is secreted by immune and vascular endothelial cells, and appears to play important roles in the pathophysiology of Kawasaki disease (KD).Thus, genetic variations in NO synthase (NOS) genes may be involved in the development of coronary artery lesions (CAL) in KD.

Methods: The present study investigated the association of endothelial constitutive NOS. The blood vessel wall is constantly exposed to mechanical forces, which have been shown to modulate its function and structure (7, 15, 28, 31, 33).Among these forces, fluid shear stress (the tractive force acting on the surface of endothelial cells as a result of blood flow) has been proposed as a key factor determining the geometric distribution of atherosclerotic lesions ().

Reduced plasma nitric oxide (NO) levels in Behçet's disease (BD) patients have been implicated in the development of the endothelial abnormalities and thrombotic complications occurring in these patients. This study investigated the association of the endothelial NO Synthase (eNOS) gene polymorphisms with BD.

Methods. A case–control study. OBJECTIVE: We previously found a T/C polymorphism in the 5'-flanking region of the endothelial nitric oxide synthase (eNOS) gene and reported that this polymorphism is strongly associated with coronary spasm.

In this study, we examined whether the polymorphism is a prognostic marker in coronary spasm patients. region of the human eNOS promoter in vascular endothelium.

Endothelial nitric-oxide synthase (eNOS)1 is the enzyme re-sponsible, in major part, for endothelial-derived NO (1). Tar-geted inactivation of the murine eNOS locus by homologous recombination and physiologic assessment of (2/2) off-spring.

GENE. Endothelial nitric oxide synthase (eNOS) is one of three isoforms of nitric oxide synthase that exhibits homology of sequence and function ().The NOS3 gene was cloned in and was localized to chromosome 7q ().Spanning kb of genomic DNA, the gene comprises 26 exons that encode a kD protein containing 1, amino acids.

The G>T polymorphism of the endothelial constitutive nitric oxide synthase gene consists of the substitution of a guanine base by a thymine at the th nucleotide of the gene. An association of this polymorphism with acute coronary syndromes has been described, only when in combination with other polymorphisms of this gene.

The. Th e constitutive class contains endothelial nitric oxide synthase (eNOS) and neuronal-NOS (nNOS), whereas another class has an inducible fo rm of NOS (iNOS) [8].

eNOS is expressed in various cell. Endothelial NOS (eNOS), also known as nitric oxide synthase 3 (NOS3) or constitutive NOS (cNOS), is an enzyme that in humans is encoded by the NOS3 gene located in the 7qq36 region of chromosome 7.

This enzyme is one of three isoforms that synthesize nitric oxide (NO), a small gaseous and lipophilic molecule that participates in several biological processes.

Zhang R. Min W, Sessa WC: Functional analysis of the human endothelial nitric oxide synthase promoter. SP1 and GATA factors are necessary for basal transcription in endothelial cells.

J Biol ChemArticle; PubMed; Google Scholar. Functional analysis of the human endothelial nitric oxide synthase promoter. Sp1 and GATA factors are necessary for basal transcription in endothelial cells. Zhang R, Min W, Sessa WC J Biol Chem. Jun (25) PubMed Article. Proc. Natl. Acad.

Sci. USA Vol. 93, pp.February Biochemistry Transcriptional regulation ofhumaninducible nitric oxide synthase (NOS2)genebycytokines: Initial analysis ofthehuman NOS2promoter (nitric oxide/tumor necrosis factor a/interleukin /interferon y/gene .Functional analysis of the human endothelial nitric oxide synthase promoter: SP1 and GATA factors ARE necessary for basal transcription in endothelial cells Article Full-text available.We evaluated the role of the neuronal constitutive (NOS1) and endothelial constitutive (NOS3) nitric oxide synthase genes and the endothelin‐1 (EDN‐1) gene in predisposition to chronic renal failure in African–Americans.

Methods.