In vivo and in vitro assessment of pathways involved in contrast media-induced renal cells apoptosis

Quintavalle, Cristina; Brenca, Monica; Micco, Francesca De; Fiore, Danilo; Romano, Simona; Romano, Maria Fiammetta; Apone, Fabio; Bianco, A. R.; Zabatta, Maria Assunta; Troncone, Giancarlo; Briguori, Carlo; Condorelli, Gerolama

doi:10.1038/cddis.2011.38

Cited by 121 publications

(125 citation statements)

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“…16 Our previous studies showed amlodipine and telmisartan could protect the renal tissue from nephrotoxicity induced by diatrizoate in rat model. 17,18 Another study indicated that enhanced formation of ROS in kidney after administration of CM play an important role in the development of CIAKI, 19 suggesting a protective effect of ROS scavenging or reducing ROS formation in CIAKI. Among these antioxidants, acetylcysteine (NAC) is the most studied agent for treatment of CIAKI.…”

Section: Discussionmentioning

confidence: 99%

Mitochondria-targeted peptides prevent on contrast-induced acute kidney injury in the rats with hypercholesterolemia

et al. 2013

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Objective: The objective of this study is to evaluate the effect and mechanism of mitochondriatargeted peptides (MTP131 and SPI20) on contrast-induced acute kidney injury (CI-AKI) in rats with hypercholesterolemia. Method: Forty SD rats were randomly divided into normal diet group (NN, n ¼ 8) and high cholesterol supplemented dietary group (HN, n ¼ 32). At the end of 8 weeks, the group HN was divided into four subgroups. All Rats were given injection of either diatrizoate (10 mL/kg) or equal volume of normal saline, the rats pretreated with MTP131 or SPI20 were given injection with MTP131 or SPI 20 (3 mg/kg) by peritoneal cavity for 3 times. Blood, urine and renal tissue samples were prepared to determine biochemical parameters. The renal pathological changes were evaluated by hematoxylin and eosin staining and scored semiquantitatively, The protein expression of renal NOX4 was also measured by Western blotting. Results: In diatrizoate-injected rats, Serum creatinine (Scr), fractional excretion of sodium (FeNa%), fractional excretion of potassium (FeK%), pathological scores, renal malondialdehyde (MDA) content, the NADPH oxidase activity and the expression of NOX4 in kidney tissue were significantly increased (p50.01). In the groups pretreated with MTP131 or SPI20, the levels of Scr, FeNa%, FeK%, MDA content and NADPH oxidase activity in renal tissue decreased (p50.01), the levels of renal super oxygen dehydrogenises and ATPase activity increased (p50.01). The renal injuries induced by contrast media (CM) were alleviated. Conclusion: MTP131 and SPI20 might protect acute kidney injury induced by CM in rats with hypercholesterolemia.

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Section: Discussionmentioning

confidence: 99%

Mitochondria-targeted peptides prevent on contrast-induced acute kidney injury in the rats with hypercholesterolemia

et al. 2013

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“…Previous studies have demonstrated that CM induce an increase in ROS production. 3,34 This leads to eventual activation of the stress kinases JNK1/2 and p38. For this reason, clinical trials have been performed with the use of various antioxidant compounds with the aim of lowering the occurrence of CIAKI by scavenging ROS.…”

Section: Mechanisms Of Prevention Of Cm-induced Renal Cell Damage Bymentioning

confidence: 99%

“…2 We have observed previously both in vitro and in vivo that CM induce apoptotic cell death via 3 important signaling pathways: (1) the reactive oxygen species (ROS) pathway, (2) the Jun N-terminal kinase (JNK)/p38 pathway, and (3) the intrinsic apoptosis pathway, which are triggered by CM in this sequence. 3,4 The causal relationship between these 3 sequential pathways supports the investigation of novel therapeutic approaches to prevent CIAKI.…”

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confidence: 99%

Impact of a High Loading Dose of Atorvastatin on Contrast-Induced Acute Kidney Injury

et al. 2012

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Background-The role of statins in the prevention of contrast-induced acute kidney injury (CIAKI) is controversial. Methods and Results-First, we investigated the in vivo effects of atorvastatin on CIAKI. Patients with chronic kidney disease enrolled in the Novel Approaches for Preventing or Limiting Events (NAPLES) II trial were randomly assigned to (1) the atorvastatin group (80 mg within 24 hours before contrast media [CM] exposure; nϭ202) or (2) the control group (nϭ208). All patients received a high dose of N-acetylcysteine and sodium bicarbonate solution. Second, we investigated the in vitro effects of atorvastatin pretreatment on CM-mediated modifications of intracellular pathways leading to apoptosis or survival in renal tubular cells. CIAKI (ie, an increase Ͼ10% of serum cystatin C concentration within 24 hours after CM exposure) occurred in 9 of 202 patients in the atorvastatin group (4.5%) and in 37 of 208 patients in the control group (17.8%) (Pϭ0.005; odds ratioϭ0.22; 95% confidence interval, 0.07-0.69). CIAKI rate was lower in the atorvastatin group in both diabetics and nondiabetics and in patients with moderate chronic kidney disease (estimated glomerular filtration rate, 31-60 mL/min per 1.73 m

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“…Various studies have demonstrated that excessive ROS promotes necroptosis in various cell types, whereas inhibiting ROS production reduces necroptosis (13)(14)(15)(16). In addition, previous studies revealed that ROS production is augmented in AKI, and that ROS lead to renal tubular epithelium injury via inflammasome activation, mitochondrion damage and tubular epithelium apoptosis (22)(23)(24)(25). To the best of our knowledge, there are no studies that have investigated the effect of ROS on necroptosis in renal tubular epithelium.…”

Section: Discussionmentioning

confidence: 99%

NADPH oxidase inhibitor, diphenyleneiodonium prevents necroptosis in HK-2 cells

Dong

Chen

et al. 2017

Biomedical Reports

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Abstract. The aim of the present study was to investigate the protective effect of the NADPH oxidase inhibitor, diphenyleneiodonium (DPI) against necroptosis in renal tubular epithelial cells. A necroptosis model of HK-2 cells was established using tumor necrosis factor-α, benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone and antimycin A (collectively termed TZA), as in our previous research. The necroptosis inhibitor, necrostatin-1 (Nec-1) or the NADPH oxidase inhibitor, DPI were administered to the necroptosis model. Production of reactive oxygen species (ROS) was detected by dichlorodihydrofluorescein diacetate in the different groups, and the manner of cell death was identified by flow cytometry. Western blot analysis was used to determine the levels of phosphorylation of receptor-interacting protein kinase 3 (RIP-3) and mixed lineage kinase domain-like (MLKL), which are essential to necroptosis. The results revealed that TZA increased the percentages of propidium iodide-positive HK-2 cells from 1.22±0.69 to 8.98±0.73% (P<0.001), and augmented the phosphorylation of RIP-3 and MLKL. ROS levels were increased in the TZA group compared with the control group (27.74±1. IntroductionAcute kidney injury (AKI) is a common clinical syndrome that is characterized by the rapid loss of kidney function and abrupt kidney damage. It is associated with high morbidity and mortality worldwide (1). Acute tubular necrosis (ATN) is the most common and severe pathological manifestation of AKI. Although necrosis has long been considered to be unregulated, previous studies have revealed various types of regulated necrosis that are independent of caspase activities (2). Necroptosis is an important type of regulated necrosis and is involved in various pathological conditions (3-7). Receptor-interacting protein kinase (RIP)-1 receives signals from various death stimuli, and subsequently recruits RIP-3 via RIP homotypic interaction motif domain-mediated interactions and promotes RIP-3 phosphorylation (8,9). Phosphorylated RIP-3 mediates the phosphorylation of mixed-lineage kinase domain-like (MLKL), ultimately leading to rupture of the plasma membrane (7). Previous studies have identified necroptosis in ATN induced by various stimuli, including ischemia/reperfusion, contrast medium and cisplatin (10-12). RIP-1 inhibition by necrostatin-1 (Nec-1), or knockout of RIP-3 or MLKL all prevent ATN (10-12).Reactive oxygen species (ROS) promote necroptosis in cardiomyocytes, liver cells, Jurkat cells and lung adenoma cells (13)(14)(15)(16). However, the effect of ROS on the necroptosis of renal tubular epithelium remains unknown. The present study hypothesized that excessive ROS production may promote necroptosis in HK-2 human kidney cells. Diphenyleneiodonium (DPI), an NADPH oxidase inhibitor, has been demonstrated to reduce ROS production and exert a protective role in numerous cell types (17)(18)(19)

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In vivo and in vitro assessment of pathways involved in contrast media-induced renal cells apoptosis

Cited by 121 publications

References 30 publications

Mitochondria-targeted peptides prevent on contrast-induced acute kidney injury in the rats with hypercholesterolemia

Mitochondria-targeted peptides prevent on contrast-induced acute kidney injury in the rats with hypercholesterolemia

Impact of a High Loading Dose of Atorvastatin on Contrast-Induced Acute Kidney Injury

NADPH oxidase inhibitor, diphenyleneiodonium prevents necroptosis in HK-2 cells

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