Pretreatment of sildenafil attenuates ischemia-reperfusion renal injury in rats

Choi, Dae Eun; Jeong, Jin Young; Lim, Beom Jin; Chung, Sarah; Chang, Yoon Kyung; Lee, Sang Ju; Na, Ki Young; Kim, Seok Young; Shin, Young Tai; Lee, Kang Wook

doi:10.1152/ajprenal.90609.2008

Cited by 109 publications

(102 citation statements)

References 42 publications

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“…Genetic mutations in parkin have been shown to be associated with familial PD (400). Although the role of parkin is still under investigation, it has been recently studied as a therapeutic for Parkinson's disease, as it is reportedly neuroprotective (1,102). UCH-L1 removes ubiquitin molecule from the Cterminal end of the poly ubiquitin polymer after attachment of the protein to the proteasome.…”

Section: Importance Of Clearance and Detoxification Systemsmentioning

confidence: 99%

Redox Proteomics in Selected Neurodegenerative Disorders: From Its Infancy to Future Applications

Butterfield

Perluigi

Reed

et al. 2012

Antioxidants & Redox Signaling

157

142

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Several studies demonstrated that oxidative damage is a characteristic feature of many neurodegenerative diseases. The accumulation of oxidatively modified proteins may disrupt cellular functions by affecting protein expression, protein turnover, cell signaling, and induction of apoptosis and necrosis, suggesting that protein oxidation could have both physiological and pathological significance. For nearly two decades, our laboratory focused particular attention on studying oxidative damage of proteins and how their chemical modifications induced by reactive oxygen species/reactive nitrogen species correlate with pathology, biochemical alterations, and clinical presentations of Alzheimer's disease. This comprehensive article outlines basic knowledge of oxidative modification of proteins and lipids, followed by the principles of redox proteomics analysis, which also involve recent advances of mass spectrometry technology, and its application to selected age-related neurodegenerative diseases. Redox proteomics results obtained in different diseases and animal models thereof may provide new insights into the main mechanisms involved in the pathogenesis and progression of oxidativestress-related neurodegenerative disorders. Redox proteomics can be considered a multifaceted approach that has the potential to provide insights into the molecular mechanisms of a disease, to find disease markers, as well as to identify potential targets for drug therapy. Considering the importance of a better understanding of the cause/effect of protein dysfunction in the pathogenesis and progression of neurodegenerative disorders, this article provides an overview of the intrinsic power of the redox proteomics approach together with the most significant results obtained by our laboratory and others during almost 10 years of research on neurodegenerative disorders since we initiated the field of redox proteomics. Antioxid. Redox Signal. 17, 1610-1655.

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Section: Importance Of Clearance and Detoxification Systemsmentioning

confidence: 99%

Redox Proteomics in Selected Neurodegenerative Disorders: From Its Infancy to Future Applications

Butterfield

Perluigi

Reed

et al. 2012

Antioxidants & Redox Signaling

157

142

View full text Add to dashboard Cite

show abstract

“…Renal injury and failure following IR injury is ameliorated by the administration of Rho kinase inhibitors [6,8,10] and other drugs [11,12,13,14], and several mechanisms may be involved. We have shown that Rho kinase inhibition prevents a decrease in endothelium-dependent vasodilation and blood flow by enhancing endothelial nitric oxide synthase (eNOS) in resistance arteries thus antagonizing the downregulation induced by renal IR injury [6,14].…”

Section: Introductionmentioning

confidence: 99%

Rho-Kinase Inhibition Reduces Early Microvascular Leukocyte Accumulation in the Rat Kidney following Ischemia-Reperfusion Injury: Roles of Nitric Oxide and Blood Flow

Versteilen

Blaauw

Maggio

et al. 2011

Nephron Exp Nephrol

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Aim: To study whether microvascular leukocyte accumulation after rat renal ischemia and reperfusion (IR) is decreased by Rho kinase inhibition, independently of effects upon nitric oxide (NO) and renal blood flow. Methods: Male Wistar rats were subjected to 60 min of ischemia by bilateral clamping and 60 min of reperfusion of the renal arteries, or a sham procedure. Haemodynamics were monitored and microsphere blood flow to the kidneys was measured. The infusion of the Rho kinase inhibitor (Y27632) was commenced before clamping and IR. The NO synthase inhibitor, N^G-nitro-L-arginine methyl ester (L-NAME), was administered after the start of reperfusion whilst the dopamine-1 receptor agonist fenoldopam, a renal vasodilator, was infused during the reperfusion period. Digital imaging microscopy analysis of cryosections was done to determine leukocyte accumulation and vasodilator-stimulated phosphoprotein serine 239 phosphorylation (p-VASP ser 239), a marker of endothelial NO. Results: Leukocytes (60–70% neutrophils) accumulated within blood vessels in the corticomedullary junction and medulla of the kidney. Leukocyte accumulation was markedly reduced by the Rho kinase inhibitor but not by fenoldopam. However, both drugs improved renal blood flow and microvascular expression of p-VASP ser 239 in the corticomedullary junction and medulla, which were decreased following IR. L-NAME treatment of IR animals pretreated with the Rho kinase inhibitor reduced blood flow and p-VASP ser 239 expression and increased leukocyte accumulation. Conclusion: Early microvascular leukocyte accumulation in the corticomedullary junction and medulla of the rat kidney after IR is ameliorated by Rho kinase inhibition. This effect is partly independent upon attenuation of decreased NO and renal blood flow.

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“…Renal function was evaluated as described previously [2]. Blood was collected from the inferior vena cava under anesthesia at sacrifice.…”

Section: Blood and Tissue Preparationmentioning

confidence: 99%

“…To measure blood urea nitrogen (BUN) and serum creatinine, aliquots of serum were analyzed using a chemistry auto-analyzer, Toshiba 200FR (Toshiba Medical Systems Co., Tokyo, Japan). Tissues were prepared as described previously [2]. Briefly, the left kidney was excised immediately after sacrifice and cut into three coronal sections.…”

Section: Blood and Tissue Preparationmentioning

confidence: 99%

Omega-3 polyunsaturated fatty acids protect against ischemia-reperfusion renal injury through AMPK-mediated autophagy

Dh¹,

Tw²,

J³

et al. 2017

Preprint

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Regulated autophagy is involved in the repair of renal ischemia-reperfusion injury (IRI). ω3-Polyunsaturated fatty acids (ω3-PUFAs) show protective effects against various renal injuries. It was recently reported that ω3-PUFAs regulate autophagy. We assessed whether ω3-PUFAs attenuated IR-induced acute kidney injury (AKI) and evaluated associated mechanisms. C57Bl/6 background fat-1 mice and wild-type mice (wt) were divided into four groups: wt sham (n = 10), fat-1 sham (n = 10), wt IRI (reperfusion 35 min after clamping both the renal artery and vein; n = 15), and fat-1 IRI (n = 15). Kidneys and blood were harvested 24 h after IRI. Renal histological and molecular data were collected. The kidneys of fat-1 mice showed better renal cell survival, renal function, and pathological damage than those of wt mice after IRI. In addition, fat-1 mice showed less oxidative stress and autophagy impairment; greater amounts of LC3, Beclin-1, and Atg7; lower amounts of p62; and higher levels of renal cathepsin D and ATP6E than wt kidneys. They also showed more AMPK activation, which resulted in the inhibition of phosphorylation of the mammalian target of rapamycin (mTOR). Collectively, ω3-PUFAs in fat-1 mice contributed to AMPK mediated autophagy activation, leading to a renoprotective response.

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Pretreatment of sildenafil attenuates ischemia-reperfusion renal injury in rats

Abstract: Shin YT, Lee KW. Pretreatment of sildenafil attenuates ischemia-reperfusion renal injury in rats.

Cited by 109 publications

References 42 publications

Redox Proteomics in Selected Neurodegenerative Disorders: From Its Infancy to Future Applications

Redox Proteomics in Selected Neurodegenerative Disorders: From Its Infancy to Future Applications

Rho-Kinase Inhibition Reduces Early Microvascular Leukocyte Accumulation in the Rat Kidney following Ischemia-Reperfusion Injury: Roles of Nitric Oxide and Blood Flow

Omega-3 polyunsaturated fatty acids protect against ischemia-reperfusion renal injury through AMPK-mediated autophagy

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