Involvement of Endogenous Interleukin-10 and Tumor Necrosis Factor-?? In Renal Ischemia-Reperfusion Injury1,2

Daemen, M.A.R.C.; Ven, M. W. C. M. Van De; Heineman, Erik; Buurman, Wim A.

doi:10.1097/00007890-199903270-00003

Cited by 142 publications

(92 citation statements)

References 46 publications

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“…Paraffin sections were stained with hematoxylin-eosin and examined histologically. The clamped kidneys displayed the characteristic morphologic changes resulting from ischemia-reperfusion injury, as previously published by others (12)(13)(14) and us (11). The other half of each kidney was embedded in OCT compound (Tissue-Tek), and frozen sections (4 m) were obtained for immunohistochemistry.…”

Section: Mouse Models Of Renal Ischemia-reperfusion Injurymentioning

confidence: 83%

“…We used well-established murine models in which the structural and functional consequences of brief periods of renal ischemia have been previously documented (11)(12)(13)(14)(15). Briefly, male Swiss-Webster mice (Taconic Farms, Germantown, NY) weighing 25 to 35 g were housed with 12:12-h light:dark cycle and were allowed free access to food and water.…”

Section: Mouse Models Of Renal Ischemia-reperfusion Injurymentioning

confidence: 99%

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Identification of Neutrophil Gelatinase-Associated Lipocalin as a Novel Early Urinary Biomarker for Ischemic Renal Injury

Mishra

Ma²,

Prada³

et al. 2003

Journal of the American Society of Nephrology

1,559

1,206

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Abstract. Acute renal failure (ARF) secondary to ischemic injury remains a common and potentially devastating problem. A transcriptome-wide interrogation strategy was used to identify renal genes that are induced very early after renal ischemia, whose protein products might serve as novel biomarkers for ARF. Seven genes that are upregulated Ͼ10-fold were identified, one of which (Cyr61) has recently been reported to be induced after renal ischemia. Unexpectedly, the induction of the other six transcripts was novel to the ARF field. In this study, one of these previously unrecognized genes was further characterized, namely neutrophil gelatinase-associated lipocalin (NGAL), because it is a small secreted polypeptide that is protease resistant and consequently might be readily detected in the urine. The marked upregulation of NGAL mRNA and protein levels in the early postischemic mouse kidney was confirmed. NGAL protein expression was detected predominantly in proliferating cell nuclear antigen-positive proximal tubule cells, in a punctate cytoplasmic distribution that colocalized with markers of late endosomes. NGAL was easily detected in the urine in the very first urine output after ischemia in both mouse and rat models of ARF. The appearance of NGAL in the urine was related to the dose and duration of renal ischemia and preceded the appearance of other urinary markers such as N-acetyl-␤-D-glucosaminidase and ␤2-microglobulin. The origin of NGAL from tubule cells was confirmed in cultured human proximal tubule cells subjected to in vitro ischemic injury, where NGAL mRNA was rapidly induced in the cells and NGAL protein was readily detectable in the culture medium within 1 h of mild ATP depletion. NGAL was also easily detectable in the urine of mice with cisplatininduced nephrotoxicity, again preceding the appearance of N-acetyl-␤-D-glucosaminidase and ␤2-microglobulin. The results indicate that NGAL may represent an early, sensitive, noninvasive urinary biomarker for ischemic and nephrotoxic renal injury.

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Section: Mouse Models Of Renal Ischemia-reperfusion Injurymentioning

confidence: 83%

Section: Mouse Models Of Renal Ischemia-reperfusion Injurymentioning

confidence: 99%

Identification of Neutrophil Gelatinase-Associated Lipocalin as a Novel Early Urinary Biomarker for Ischemic Renal Injury

Mishra

Ma²,

Prada³

et al. 2003

Journal of the American Society of Nephrology

1,559

1,206

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“…α -hANP attenuates I/R injury at least in part by reducing the activation of neutrophils in the kidney. TNF alpha production is enhanced in I/R-induced renal injury (Daemen et al 1999). TNF alpha activates neutrophils to promote the release of inflammatory mediators like CINC-1.…”

Section: Discussionmentioning

confidence: 99%

Atrial Natriuretic Peptide Attenuates Ischemia/Reperfusion-Induced Renal Injury by Reducing Neutrophil Activation in Rats

Chujo

Ueki

Asaga

et al. 2008

Tohoku J. Exp. Med.

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Activated neutrophils have been implicated in the development of ischemia/reperfusion (I/R)-induced renal failure. Cytokine-induced neutrophil chemoattractant-1 (CINC-1), a major factor in acute inflammation, is responsible for the activation of neutrophils and for neutrophil chemotaxis to sites of injury. Atrial natriuretic peptide (ANP), a hormone synthesized by the cardiac atria, was shown to possess anti-inflammatory potential due to its potency to inhibit the production of inflammatory mediators. We examined whether the human form of ANP attenuates I/R-induced renal injury by reducing neutrophil activation in a rat model. Male Wistar rats weighing 200-240 g were observed for 24 h after reperfusion following 45-min renal ischemia. Rats were intravenously administered alphahuman ANP (α -hANP, 0.2 μ g/kg/min) beginning immediately after ischemia and continuing for 2 h after reperfusion. CINC-1 and myeloperoxidase (MPO) concentrations were measured to assess activation of the infiltrating neutrophil. Blood urea nitrogen and serum creatinine and urinary N-acetyl β -d-glucosaminidase (NAG) were measured as indicators of glomerular function and as a specific indicator of proximal tubular function, respectively. α -hANP significantly inhibited I/R-induced increases in renal CINC-1 and MPO concentrations. α -hANP also reduced I/R-induced increases in the concentrations of blood urea nitrogen and serum creatinine, and improved histopathologic changes, including acute tubular necrosis. These findings indicate that α -hANP attenuates I/R-induced acute renal injury, at least in part by reducing neutrophil activation, and may be useful in surgeries, associated with renal ischemia, as well as in renal transplantation.human atrial natriuretic peptide; neutrophils; kidney; ischemia/reperfusion; cytokine-induced neutrophil chemoattractant-1. Tohoku

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“…This regulation may be as a result of increased production of cytokines such as tumor necrosis factor (TNF)-α and growth factors such as hepatocyte growth factor (HGF) produced by extrarenal organs [7] . In addition, there is an inflammatory response to renal ischemia that results in secondary injury [8] . Further more, renal ischemia results in increased interleukin (IL)-6 mRNA expression [9] , renal production of IL-6, and expression of IL-10 receptors.…”

Section: Introductionmentioning

confidence: 99%

Effects of different periods of renal ischemia on liver as a remote organ

Kadkhodaee

Golab²,

Zahmatkesh³

et al. 2009

WJG

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AIM:To assess the hepatic changes after induction of different periods of renal ischemia. METHODS:Rats were subjected to either sham operation or ischemia (30, 45 and 60 min) followed by 60 min reperfusion. Liver and renal functional indices were measured. Hepatic glutathione (GSH) and ferric reducing antioxidant power levels and the concentration of interleukin (IL)-10 and tumor necrosis factor (TNF-α) were evaluated. Portions of liver and kidney tissues were fixed for histological evaluation. RESULTS:Forty-five minutes renal ischemia followed by 60 min reperfusion caused significant changes in liver structure and a significant reduction in renal function. These rats showed a significant decrease in liver GSH, as well as a significant increase in TNF-α and IL-10 concentrations. These results demonstrated that renal ischemia caused changes in liver histology, function, oxidative stress and inflammatory status, which led to a reduction in hepatic antioxidant capacity. With 30 min ischemia, the magnitude of these changes was less than those with 45 or 60 min ischemia. CONCLUSION:A minimum of 45 min ischemia is needed to study the effects of renal injury on the liver as a remote organ.

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Involvement of Endogenous Interleukin-10 and Tumor Necrosis Factor-?? In Renal Ischemia-Reperfusion Injury1,2

Cited by 142 publications

References 46 publications

Identification of Neutrophil Gelatinase-Associated Lipocalin as a Novel Early Urinary Biomarker for Ischemic Renal Injury

Identification of Neutrophil Gelatinase-Associated Lipocalin as a Novel Early Urinary Biomarker for Ischemic Renal Injury

Atrial Natriuretic Peptide Attenuates Ischemia/Reperfusion-Induced Renal Injury by Reducing Neutrophil Activation in Rats

Effects of different periods of renal ischemia on liver as a remote organ

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