Early effects of diabetes on inducible nitric oxide synthase in the kidney

Cosenzi, Alessandro; Bernobich, Elena; Bonavita, M.; Trevisan, Roberto; Bellini, Giuseppe; Campanacci, L

doi:10.1007/s005920200019

Cited by 27 publications

(27 citation statements)

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“…In support to that, Dias et al have reported that the iNOS expression in cardiac myocytes is induced following pathological situations where it contributes to myocardial dysfunction [22]. Cosenzi et al have shown that following to the induction of diabetes in rats, iNOS is activated in their kidney which is suggestive of the protective role of NO observed in diabetes where NO may be involved in inducing glomerular filtration observed in diabetic patients [23].…”

Section: Discussionmentioning

confidence: 78%

Effect of Exercise Training on the Expression of p53 and iNOS in the Cardiac Muscle of Type I Diabetic Rats

Al-Jarrah

2012

J Endocrinol Metab

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Background: Diabetes is associated with a marked increase in the risk of cardiac diseases, including atherosclerosis, cardiomyopathy, and impaired ventricular function. The ability of exercise to reduce the risk of cardiac troubles has been established, but no studies have examined this link in type 1 diabetes. A randomized, controlled animal study was designed using a standard rat model of type 1 diabetes. The goal of this study was to investigate the expression of P53 and iNOS in cardiac muscle of rat with Alloxan-induced diabetes.

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Section: Discussionmentioning

confidence: 78%

Effect of Exercise Training on the Expression of p53 and iNOS in the Cardiac Muscle of Type I Diabetic Rats

Al-Jarrah

2012

J Endocrinol Metab

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“…The source of NO for the reaction with superoxide to form peroxynitrite in the diabetic rat kidney is not known, and there have been variable reports of the renal expression of NOS isoforms in diabetes. Thus, Cosenzi et al (2002) found increased iNOS in the kidney of diabetic rats, and iNOS expression was increased in endothelial cells exposed to high glucose (Rodriguez et al, 2006). In contrast, Veelken et al (2000) reported increased endothelial NOS in glomeruli from diabetic rats, and Ito et al (2001) reported increased renal neuronal NOS mRNA.…”

Section: Fenofibrate and Renal Cox-2 In Diabetes 661mentioning

confidence: 93%

Fenofibrate Treatment of Diabetic Rats Reduces Nitrosative Stress, Renal Cyclooxygenase-2 Expression, and Enhanced Renal Prostaglandin Release

Chen¹,

Quilley²

2007

J Pharmacol Exp Ther

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Renal cyclooxygenase (COX)-2 expression is increased in the diabetic rat and has been linked to increased glomerular filtration rate (GFR) and renal injury. Our studies indicate that oxidative stress in the form of peroxynitrite (ONOO) may be the stimulus for induction of COX-2. In this study, we addressed the effects of a peroxisome proliferator-activated receptor ␣ agonist on renal COX-2 expression as fibrates exert renal protective effects. Forty-eight hours after the induction of diabetes with streptozotocin in male Wistar rats, fenofibrate treatment (100 mg/kg/day) was started, and the effects were compared with untreated diabetic rats and treated and untreated agematched control rats (n ϭ 5 per group). After 12 to 14 weeks of treatment, the right kidney was perfused to determine prostaglandin release in response to arachidonic acid (AA), and the left kidney was used to examine the expression of COX-2 and nitrotyrosine, an index of ONOO formation. Release of prostaglandin (PG) E 2 in response to AA was enhanced in the diabetic rat kidney compared with control (4.8 Ϯ 0.7 versus 1.9 Ϯ 0.7 ng/min) and reduced by fenofibrate to 0.6 Ϯ 0.2 ng/min. A similar pattern was obtained for AA-stimulated release of 6-ketoPGF 1␣ . The effects of fenofibrate were associated with reduced renal expression of COX-2 and nitrotyrosine in diabetic rats. We used creatinine clearance as an index of GFR, which was increased in the diabetic rat, 3.09 Ϯ 0.4 versus 1.15 Ϯ 0.1 ml/min for control, and reduced by fenofibrate treatment to 1.87 Ϯ 0.3 ml/min. These results show that fenofibrate treatment of diabetic rats decreases renal COX-2 expression, possibly by reducing nitrosative stress, and is associated with a reduction of the enhanced GFR.

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“…The results of this study do not mean that superoxide is the mediator of COX-2-induction, only that is plays a central role. Thus, NO formation is also increased in the diabetic kidney (Sugimoto et al, 1998;Cosenzi et al, 2002;Onozato et al, 2002), and its product upon reaction with superoxide, i.e., peroxynitrite, has also been reported to induce COX-2 (Eligini et al, 2001;Nedelec et al, 2001). That peroxynitrite formation is increased in diabetes is apparent from increased staining for nitrotyrosine (Thuraisingham et al, 2000;Onozato et al, 2002), and preliminary data from our laboratory showing increased renal expression of nitrotyrosine support these results.…”

Section: Tempol Oxidative Stress and Renal Cox-2 In Diabetes 823mentioning

confidence: 99%

Effect of Tempol on Renal Cyclooxygenase Expression and Activity in Experimental Diabetes in the Rat

Chen²,

Quilley³

2005

J Pharmacol Exp Ther

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Renal cyclooxygenase (COX)-2 expression is increased in the streptozotocin (STZ)-diabetic rat and is associated with enhanced renal prostaglandin release in response to arachidonic acid (AA). Endoperoxide-mediated vasoconstrictor responses to AA were also enhanced in the diabetic rat kidney. Because oxidative stress is increased in diabetes and has been shown to induce COX-2, we assessed its contribution to prostaglandin release by treating diabetic rats with tempol (120 mg/kg/day) for 28 days. Release of AA-stimulated prostaglandins PGE 2 and 6-ketoPGF 1␣ from the isolated perfused kidney was used as an index of COX activity, and Western analysis was used to determine COX-2 protein expression. In untreated diabetic rats, the release of prostaglandins in response to AA was markedly enhanced; the increase in release of both 6-ketoPGF 1␣ and PGE 2 after AA was twice that in control rats. Renal cortical COX-2 expression in diabetic rats was 3-fold that of control rats. Tempol treatment reduced the AA-stimulated release of prostaglandins to levels seen in control rats; this was associated with reduced expression of COX-2 protein to levels not different from that in control rats. However, the enhanced vasoconstrictor response to AA in diabetic rats was unaffected by tempol treatment but abolished by inhibition of COX-1 with SC58560 [5-(4-chlorophenyl)-1-(4-methoxyphenyl)-3-(trifluoromethyl)-1H-pyrazole]. The addition of tempol to the perfusate of kidneys from diabetic and control rats had only a slight effect on prostaglandin release. We conclude that oxidative stress is an integral component of the mechanism involved in the induction of renal COX-2 in diabetes.

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Early effects of diabetes on inducible nitric oxide synthase in the kidney

Cited by 27 publications

References 0 publications

Effect of Exercise Training on the Expression of p53 and iNOS in the Cardiac Muscle of Type I Diabetic Rats

Effect of Exercise Training on the Expression of p53 and iNOS in the Cardiac Muscle of Type I Diabetic Rats

Fenofibrate Treatment of Diabetic Rats Reduces Nitrosative Stress, Renal Cyclooxygenase-2 Expression, and Enhanced Renal Prostaglandin Release

Effect of Tempol on Renal Cyclooxygenase Expression and Activity in Experimental Diabetes in the Rat

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