Cadmium-Induced Renal Cell Toxicity Is Associated With MicroRNA Deregulation

Lemaire, Joannie; Hauwaert, Cynthia Van der; Savary, Grégoire; Dewaeles, Edmone; Perrais, Michaël; Guidice, J.‐M. Lo; Pottier, Nicolas; Glowacki, François; Cauffiez, Christelle

doi:10.1177/1091581819899039

Cited by 17 publications

(5 citation statements)

References 84 publications

(92 reference statements)

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“…Cell culture. RPTECs (renal proximal tubular epithelial cells) immortalized with a pLXSN-hTERT1 retroviral vector (CRL-4031, ATCC) are a relevant in vitro model to evaluate cisplatin’s deleterious effects [ 34 , 35 , 36 ]. Cells were cultured in DMEM-F12 medium (Thermo Fisher Scientific, Waltham, MA, USA) supplemented with 1% penicillin–streptomycin, 5 pmol/L triiodo-l-thyronine, 10 ng/mL recombinant human EGF, 3.5 μg/mL ascorbic acid, 5.0 μg/mL human transferrin, 5.0 μg/mL insulin, 25 ng/mL prostaglandin E1, 25 ng/mL hydrocortisone, 8.65 ng/mL sodium selenite, 0.1 mg/mL G418, and 1.2 g/L sodium bicarbonate (Sigma Aldrich, St. Louis, MO, USA).…”

Section: Methodsmentioning

confidence: 99%

Daily Caffeine Consumption May Increase the Risk of Acute Kidney Injury Related to Platinum-Salt Chemotherapy in Thoracic Cancer Patients: A Translational Study

Hamroun,

Decaestecker,

Larrue

et al. 2024

Nutrients

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Although their efficacy has been well-established in Oncology, the use of platinum salts remains limited due to the occurrence of acute kidney injury (AKI). Caffeine has been suggested as a potential pathophysiological actor of platinum-salt-induced AKI, through its hemodynamic effects. This work aims to study the association between caffeine consumption and the risk of platinum-salt-induced AKI, based on both clinical and experimental data. The clinical study involved a single-center prospective cohort study including all consecutive thoracic cancer patients receiving a first-line platinum-salt (cisplatin or carboplatin) chemotherapy between January 2017 and December 2018. The association between daily caffeine consumption (assessed by a validated auto-questionnaire) and the risk of platinum-salt induced AKI or death was estimated by cause-specific Cox proportional hazards models adjusted for several known confounders. Cellular viability, relative renal NGAL expression and/or BUN levels were assessed in models of renal tubular cells and mice co-exposed to cisplatin and increasing doses of caffeine. Overall, 108 patients were included (mean age 61.7 years, 65% men, 80% tobacco users), among whom 34 (31.5%) experienced a platinum-salt-induced AKI (67% Grade 1) over a 6-month median follow-up. The group of high-caffeine consumption (≥386 mg/day) had a two-fold higher hazard of AKI (adjusted HR [95% CI], 2.19 [1.05; 4.57]), without any significant association with mortality. These results are consistent with experimental data confirming enhanced cisplatin-related nephrotoxicity in the presence of increasing doses of caffeine, in both in vitro and in vivo models. Overall, this study suggests a potentially deleterious effect of high doses of daily caffeine consumption on the risk of platinum-salt-related AKI, in both clinical and experimental settings.

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Section: Methodsmentioning

confidence: 99%

Daily Caffeine Consumption May Increase the Risk of Acute Kidney Injury Related to Platinum-Salt Chemotherapy in Thoracic Cancer Patients: A Translational Study

Hamroun,

Decaestecker,

Larrue

et al. 2024

Nutrients

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“…RPTECs immortalized with a pLXSN-hTERT1 retroviral vector (CRL-4031, ATCC) are a relevant in vitro model to evaluate cisplatin’s deleterious effects ( 73 – 75 ). Cells were cultured in DMEM with F12 medium (DMEM and Ham’s F12 Medium, Thermo Fisher Scientific) supplemented with 1% penicillin-streptomycin, 5 pmol/L triiodo- l -thyronine, 10 ng/mL recombinant human EGF, 3.5 μg/mL ascorbic acid, 5.0 μg/mL human transferrin, 5.0 μg/mL insulin, 25 ng/mL prostaglandin E1, 25 ng/mL hydrocortisone, 8.65 ng/mL sodium selenite, 0.1 mg/mL G418, and 1.2 g/L sodium bicarbonate (MilliporeSigma).…”

Section: Methodsmentioning

confidence: 99%

Istradefylline protects from cisplatin-induced nephrotoxicity and peripheral neuropathy while preserving cisplatin antitumor effects

Dewaeles¹,

Carvalho²,

Fellah³

et al. 2022

Journal of Clinical Investigation

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Cisplatin is a potent chemotherapeutic drug that is widely used in the treatment of various solid cancers. However, its clinical effectiveness is strongly limited by frequent severe adverse effects, in particular nephrotoxicity and chemotherapy-induced peripheral neuropathy. Thus, there is an urgent medical need to identify novel strategies that limit cisplatin-induced toxicity. In the present study, we show that the FDA-approved adenosine A 2A receptor antagonist istradefylline (KW6002) protected from cisplatin-induced nephrotoxicity and neuropathic pain in mice with or without tumors. Moreover, we also demonstrate that the antitumoral properties of cisplatin were not altered by istradefylline in tumor-bearing mice and could even be potentiated. Altogether, our results support the use of istradefylline as a valuable preventive approach for the clinical management of patients undergoing cisplatin treatment.

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“…The EVs contain and transfer a wide range of nucleic acids, among which mRNA, miRNAs, and long noncoding RNAs (lncRNAs) are the most common [ 40 , 41 , 42 ]. miRNAs are short non-coding, single-stranded RNA molecules with an average of 22 nucleotides in length and have the particularity to be highly conserved sequences between species [ 41 ].…”

Section: Evs In Kidneysmentioning

confidence: 99%

Extracellular Vesicles in Redox Signaling and Metabolic Regulation in Chronic Kidney Disease

et al. 2022

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Chronic kidney disease (CKD) is a world health problem increasing dramatically. The onset of CKD is driven by several mechanisms; among them, metabolic reprogramming and changes in redox signaling play critical roles in the advancement of inflammation and the subsequent fibrosis, common pathologies observed in all forms of CKD. Extracellular vesicles (EVs) are cell-derived membrane packages strongly associated with cell-cell communication since they transfer several biomolecules that serve as mediators in redox signaling and metabolic reprogramming in the recipient cells. Recent studies suggest that EVs, especially exosomes, the smallest subtype of EVs, play a fundamental role in spreading renal injury in CKD. Therefore, this review summarizes the current information about EVs and their cargos’ participation in metabolic reprogramming and mitochondrial impairment in CKD and their role in redox signaling changes. Finally, we analyze the effects of these EV-induced changes in the amplification of inflammatory and fibrotic processes in the progression of CKD. Furthermore, the data suggest that the identification of the signaling pathways involved in the release of EVs and their cargo under pathological renal conditions can allow the identification of new possible targets of injury spread, with the goal of preventing CKD progression.

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Cadmium-Induced Renal Cell Toxicity Is Associated With MicroRNA Deregulation

Cited by 17 publications

References 84 publications

Daily Caffeine Consumption May Increase the Risk of Acute Kidney Injury Related to Platinum-Salt Chemotherapy in Thoracic Cancer Patients: A Translational Study

Daily Caffeine Consumption May Increase the Risk of Acute Kidney Injury Related to Platinum-Salt Chemotherapy in Thoracic Cancer Patients: A Translational Study

Istradefylline protects from cisplatin-induced nephrotoxicity and peripheral neuropathy while preserving cisplatin antitumor effects

Extracellular Vesicles in Redox Signaling and Metabolic Regulation in Chronic Kidney Disease

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