Nitric oxide prevents apoptosis of human endothelial cells from high glucose exposure during early stage

Ho, Feng Ming; Liu, Shing‐Hwa; Liau, Chiau Suong; Huang, Pang-Shuo; Shiah, Shine-Gwo; Lin‐Shiau, Shoei‐Yn

doi:10.1002/(sici)1097-4644(19991101)75:2<258::aid-jcb8>3.0.co;2-3

Cited by 57 publications

(20 citation statements)

References 30 publications

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“…NO may attenuate H 2 O 2 production by inducing catalase. In agreement with this idea, it has been demonstrated that NO decreases H 2 O 2 production induced by lectin in human polymorphonuclear leukocytes, reduces H 2 O 2 generation by TNF-␣ treatment of carcinomas, inhibits H 2 O 2 production by high glucose exposure in HUVEC, and decreases the degree of elevation of H 2 O 2 induced by insulin-like growth factor I in cultured rat aortic smooth muscle cells (55)(56)(57)(58). H 2 O 2 has been shown to act as a signaling molecule that activates transcriptional factor NF-B, which then mediates the expression of proinflammatory cytokines in macrophages stimulated by LPS (59 -61).…”

Section: Discussionmentioning

confidence: 67%

Nitric Oxide Protects Macrophages from Hydrogen Peroxide-Induced Apoptosis by Inducing the Formation of Catalase

Yoshioka

Kitao

Kishino

et al. 2006

The Journal of Immunology

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We investigated the cytoprotective effect of NO on H2O2-induced cell death in mouse macrophage-like cell line RAW264. H2O2-treated cells showed apoptotic features, such as activation of caspase-9 and caspase-3, nuclear fragmentation, and DNA fragmentation. These apoptotic features were significantly inhibited by pretreatment for 24 h with NO donors, sodium nitroprusside and 1-hydroxy-2-oxo-3,3-bis-(2-aminoethyl)-1-triazene, at a low nontoxic concentration. The cytoprotective effect of NO was abrogated by the catalase inhibitor 3-amino-1,2,4-triazole but was not affected by a glutathione synthesis inhibitor, l-buthionine-(S,R)-sulfoximine. NO donors increased the level of catalase and its activity in a concentration-dependent manner. Cycloheximide, a protein synthesis inhibitor, inhibited both the NO-induced increase in the catalase level and the cytoprotective effect of NO. These results indicate that NO at a low concentration protects macrophages from H2O2-induced apoptosis by inducing the production of catalase.

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Section: Discussionmentioning

confidence: 67%

Nitric Oxide Protects Macrophages from Hydrogen Peroxide-Induced Apoptosis by Inducing the Formation of Catalase

Yoshioka

Kitao

Kishino

et al. 2006

The Journal of Immunology

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“…Salt and co-workers reported that chronic elevated glucose reduced eNOS activity in the absence of changes in eNOS phosphorylation [30]. Ho and colleagues reported that eNOS protein expression in HUVECs was up-regulated by acute high glucose (33 mmol/l) exposure for 2 to 6 h, and gradually decreased after longer exposure [31]. Conversely, Cosentino et al have reported the up-regulation of eNOS expression after the exposure of human aortic ECs to 22 mmol/l glucose for 5 days [11].…”

Section: Discussionmentioning

confidence: 99%

Hyperglycaemia-induced superoxide production decreases eNOS expression via AP-1 activation in aortic endothelial cells

et al. 2004

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Aims/hypothesis. Hyperglycaemia is a primary cause of vascular complications in diabetes. A hallmark of these vascular complications is endothelial cell dysfunction, which is partly due to the reduced production of nitric oxide. The aim of this study was to investigate the regulation of endothelial nitric oxide synthase (eNOS) activity by acute and chronic elevated glucose. Methods. Human aortic endothelial cells were cultured in 5.5 mmol/l (NG) or 25 mmol/l glucose (HG) for 4 h, 1 day, 3 days or 7 days. Mouse aortic endothelial cells were freshly isolated from C57BL/6J control and diabetic db/db mice. The expression and activity of eNOS were measured using quantitative PCR and nitrite measurements respectively. The binding of activator protein-1 (AP-1) to DNA in nuclear extracts was determined using electrophoretic mobility-shift assays. Results. Acute exposure (4 h) of human aortic endothelial cells to 25 mmol/l glucose moderately increased eNOS activity and eNOS mRNA and protein expression. In contrast, chronic exposure to elevated glucose (25 mmol/l for 7 days) reduced total nitrite levels (46% reduction), levels of eNOS mRNA (46% reduction) and eNOS protein (65% reduction). In addition, AP-1 DNA binding activity was increased in chronic HGcultured human aortic endothelial cells, and this effect was reduced by the specific inhibition of reactive oxygen species production through the mitochondrial electron transport chain. Mutation of AP-1 sites in the human eNOS promoter reversed the effects of HG. Compared with C57BL/6J control mice, eNOS mRNA levels in diabetic db/db mouse aortic endothelial cells were reduced by 60%. This decrease was reversed by the overexpression of manganese superoxide dismutase using an adenoviral construct. Conclusions/interpretation. In diabetes, the expression and activity of eNOS is regulated through glucosemediated mitochondrial production of reactive oxygen species and activation of the oxidative stress transcription factor AP-1. Abbreviations: AP-1, activator protein-1 · EC, endothelial cell · eNOS, endothelial nitric oxide synthase · FBS, fetal bovine serum · HG, high glucose · MnSOD, manganese superoxide dismutase · MOI, multiplicity of infection · NF-κB, nuclear factor-κB · NG, normal glucose · ROS, reactive oxygen species · UCP-1, uncoupling protein-1

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“…Evidence for increased NO production under hyperglycemic conditions is shown, for example, by the increase in NO release in endothelial cells exposed to high glucose levels (9,16,18). Furthermore, indices of NO production such as nitrate and nitrite levels are elevated in experimentally induced models of diabetes (3,31).…”

Section: Discussionmentioning

confidence: 99%

Hypertension inl-NAME-treated diabetic rats depends on an intact sympathetic nervous system

Fitzgerald

Brands

2002

American Journal of Physiology-Regulatory, Integrative and Comp

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Fitzgerald, Sharyn M., and Michael W. Brands. Hypertension in L-NAME-treated diabetic rats depends on an intact sympathetic nervous system. Am J Physiol Regulatory Integrative Comp Physiol 282: R1070-R1076, 2002. First published November 23, 2001 10.1152/ajpregu.00468. 2001.-We demonstrated previously that induction of diabetes in rats that were treated chronically with the nitric oxide synthase inhibitor N G -nitro-L-arginine methyl ester (L-NAME) causes a severe, progressive increase in mean arterial pressure. This study tested the role of the sympathetic nervous system in that response. Rats were instrumented with chronic artery and vein catheters and assigned randomly to four diabetic groups pretreated with vehicle (D), L-NAME (DϩL), the ␣1-and ␤-adrenergic receptor antagonists terazosin and propranolol (DϩB), or L-NAME, terazosin, and propranolol (DϩLB). After baseline measurements were taken, rats were pretreated; 6 days later, streptozotocin was administered and 3 wk of diabetes ensued. DϩL rats had a marked, progressive increase in arterial pressure that by day 20 was ϳ60 mmHg greater than in D rats. The pressor response to L-NAME was significantly attenuated in diabetic rats cotreated with adrenergic blockers. During week 1 of diabetes, plasma renin activity (PRA) increased and then returned to control levels in D rats. PRA increased progressively in DϩL rats, and chronic adrenergic receptor blockade restored the biphasic renin response in DϩLB rats. These results suggest that the sympathetic nervous system may be involved in the hypertensive response to onset of diabetes in L-NAME-treated rats, possibly through control of renin secretion. nitric oxide; mean arterial pressure; glucose; angiotensin II; glomerular filtration rate; N G -nitro-L-arginine methyl ester DIABETES GENERALLY IS ASSOCIATED with an impairment in endothelial function (10,34,35,37,43). The long-term consequences of this impairment have not been well established, but it may play an important role in the accelerated atherosclerosis and increased prevalence of cardiovascular disease that is observed in diabetic populations (45a). Also unclear is what role the endothelium and its vasoactive hormones play in circulatory homeostasis early in diabetes before significant impairment develops (4,20,34,44). We demonstrated recently (15) that the induction of diabetes in the absence of a functional nitric oxide (NO) system causes a severe, progressive increase in mean arterial pressure (MAP). This finding suggests that there may be increased dependence on NO in the early stages of diabetes such that NO is essential to prevent hypertension from developing. This is consistent with reports (10, 31) that NO production is increased during the early stages of diabetes.The mechanism for this potentiating interaction on blood pressure between induction of diabetes and chronic NO synthesis inhibition is not known, but a role for the renin-angiotensin system was implicated by the finding of increased plasma renin activity (PRA) in the rats in our study ...

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Nitric oxide prevents apoptosis of human endothelial cells from high glucose exposure during early stage

Cited by 57 publications

References 30 publications

Nitric Oxide Protects Macrophages from Hydrogen Peroxide-Induced Apoptosis by Inducing the Formation of Catalase

Nitric Oxide Protects Macrophages from Hydrogen Peroxide-Induced Apoptosis by Inducing the Formation of Catalase

Hyperglycaemia-induced superoxide production decreases eNOS expression via AP-1 activation in aortic endothelial cells

Hypertension inl-NAME-treated diabetic rats depends on an intact sympathetic nervous system

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