NO and NOS isoforms in the development of apoptosis in renal ischemia/reperfusion

Viñas, Jose Luis; Solà, Anna; Genescà, Meritxell; Alfaro, Vicente; Pi, Felip; Hotter, Georgina

doi:10.1016/j.freeradbiomed.2005.10.046

Cited by 81 publications

(90 citation statements)

References 37 publications

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“…In addition, FGF has been reported to inhibit EPO-induced erythropoiesis (Schmerer et al, 2006;Kreja et al, 1993). It is possible that the observed EPO induction in ischemic kidneys treated with FGFR2-ASO could be related to the molecular machinery Recent studies have shown that nitric oxide (NO) generated by iNOS is involved in many pathological states (including renal I/R), contributing to oxidative damage of critical cellular macromolecules (Chatterjee et al, 2002;Viñas et al, 2006). In addition, the increase in HO-1, together with an increase in iNOS, the former producing CO and the latter producing NO, could contribute to the production of NO in a regulated and benefi cial form (Lee and Yen, 2009).…”

Section: Discussionmentioning

confidence: 99%

Cyclooxygenase-2 and hypoxia-regulated proteins are modulated by basic fibroblast growth factor in acute renal failure

et al. 2012

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Acute renal failure (ARF) can be caused by injuries that induce tissue hypoxia, which in turn can trigger adaptive or infl ammatory responses. We previously showed the participation of basic fi broblast growth factor (FGF-2) in renal repair. Based on this, the aim of this study was to analyze the effect of FGF-2 signaling pathway manipulation at hypoxia-induced protein levels, as well as in key proteins from the vasoactive systems of the kidney. We injected rat kidneys with FGF-2 recombinant protein (r-FGF) or FGF-2 receptor antisense oligonucleotide (FGFR2-ASO) after bilateral ischemia, and evaluated the presence of iNOS, EPO and HO-1, in representation of hypoxiainduced proteins, as well as COX-2, renin, kallikrein, and B2KR, in representation of the vasoactive systems of the kidney. A reduction in iNOS, HO-1, EPO, renin, kallikrein, B2KR, and in renal damage was observed in animals treated with r-FGF. The opposite effect was found with FGF-2 receptor down-regulation. In contrast, COX-2 protein levels were higher in kidneys treated with r-FGF and lower in those that received FGFR2-ASO, as compared to saline treated kidneys. These res ults suggest that the protective role of FGF-2 in the pathogenesis of ARF induced by I/R is a complex process, through which a differential regulation of metabolic pathways takes place.

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Section: Discussionmentioning

confidence: 99%

Cyclooxygenase-2 and hypoxia-regulated proteins are modulated by basic fibroblast growth factor in acute renal failure

et al. 2012

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“…It is known that during renal I/R injury, apoptosis is a very important contributor to kidney damage. While evaluating experimentally created I/R, Vinas et al demonstrated that the cells died of apoptosis or necrosis according to the severity of the injury, due to direct cellular damage caused by free oxygen radicals (17). In accordance with this study, an increase in the number of apoptotic cells subsequent to the renal I/R injury was observed in our investigation; however, this increase was prevented by quercetin treatment and this was due to the anti-apoptotic effect of quercetin.…”

Section: Discussionmentioning

confidence: 99%

“…Conversely, there are studies which demonstrate that the increased activity of NOS is associated with reduced I/R-induced injury (25). Alterations in the expression of various NOS isoforms have been described in renal I/R injury (17). Vinas et al reported that, according to quantitative analysis, I/R increased the renal expression of iNOS compared to the control and that no differences were found between I/R and the various selective NOS inhibitors (17).…”

Section: Discussionmentioning

confidence: 99%

“…Alterations in the expression of various NOS isoforms have been described in renal I/R injury (17). Vinas et al reported that, according to quantitative analysis, I/R increased the renal expression of iNOS compared to the control and that no differences were found between I/R and the various selective NOS inhibitors (17). In the present study, quantitative iNOS expression increased in the I/R group and no significant difference was observed between the I/R and quercetin treatment groups, similar to the Vinas et al study.…”

Section: Discussionmentioning

confidence: 99%

“…NO is produced by constitutive NO synthases (cNOSs), including endothelial NOS (eNOS), neuronal NOS (nNOS) and inducible NOS (iNOS). Alterations in the expression/activity of the different NOS isoforms have been described in renal I/R (17). However, no study has been found which simultaneously investigates the effects of quercetin on p53, apoptosis, NF-κB and NOS gene expression in renal I/R injury.…”

Section: Introductionmentioning

confidence: 99%

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Effects of quercetin on apoptosis, NF-κB and NOS gene expression in renal ischemia/reperfusion injury

Kinaci

Erkasap

Küçük

et al. 2011

Experimental and Therapeutic Medicine

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Abstract. The aim of this study was to investigate the effects of quercetin on nitric oxide synthase (NOS), nuclear factor-κB (NF-κB) and apoptosis in renal ischemia/reperfusion (I/R) injury in rats. A total of 42 Sprague-Dawley rats were divided into three groups. The control, I/R and I/R+quercetin (I/R+Q) groups were treated with quercetin (50 mg/kg intraperitoneal) 1 h prior to the induction of ischemia. Tissue malondialdehyde (MDA) and glutathione (GSH) levels were determined by high-performance liquid chromatography (HPLC). p53, endothelial NOS (eNOS) and NF-κB expression were assessed immunohistochemically, and apoptosis assesment was performed using terminal deoxy nucleotidyl transferase dUTP nick end-labeling (TUNEL) assay. The mRNA levels of inducible NOS (iNOS) in renal tissue were determined by realtime polymerase chain reaction (RT-PCR). MDA levels were significantly decreased in the quercetin group compared to the I/R group. However, GSH levels were significantly increased with quercetin treatment in the I/R group. Histological results, the number of apoptotic and p53-positive cells, NF-κB and eNOS expression levels were significantly decreased in the quercetin treatment group compared to the I/R group. iNOS gene expression increased in the I/R group, but no significant difference was found between the I/R and quercetin treatment groups. Therefore, quercetin not only has antioxidant and antiapoptotic activities, but also has an inhibitory effect on eNOS and NF-κB for renal tissue protection during I/R injury in rats. Therefore, quercetin may be a promising renoprotective therapeutic agent.

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Nitric Oxide Therapy for Diabetic Wound Healing

Malone-Povolny

Maloney

Schoenfisch

2019

Adv Healthcare Materials

273

221

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Nitric oxide (NO) represents a potential wound therapeutic agent due to its ability to regulate inflammation and eradicate bacterial infections. Two broad strategies exist to utilize NO for wound healing; liberating NO from endogenous reservoirs, and supplementing NO from exogenous sources. This progress report examines the efficacy of a variety of NO‐based methods to improve wound outcomes, with particular attention given to diabetes‐associated chronic wounds.

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NO and NOS isoforms in the development of apoptosis in renal ischemia/reperfusion

Cited by 81 publications

References 37 publications

Cyclooxygenase-2 and hypoxia-regulated proteins are modulated by basic fibroblast growth factor in acute renal failure

Cyclooxygenase-2 and hypoxia-regulated proteins are modulated by basic fibroblast growth factor in acute renal failure

Effects of quercetin on apoptosis, NF-κB and NOS gene expression in renal ischemia/reperfusion injury

Nitric Oxide Therapy for Diabetic Wound Healing

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