Working Paper Article Version 1 This version is not peer-reviewed

RIP3-Dependent Necroptosis Promotes Cisplatin-Induced Ototoxicity

Version 1 : Received: 19 March 2019 / Approved: 19 March 2019 / Online: 19 March 2019 (10:40:20 CET)

A peer-reviewed article of this Preprint also exists.

Choi, M.-J.; Kang, H.; Lee, Y.Y.; Choo, O.-S.; Jang, J.H.; Park, S.-H.; Moon, J.-S.; Choi, S.J.; Choung, Y.-H. Cisplatin-Induced Ototoxicity in Rats Is Driven by RIP3-Dependent Necroptosis. Cells 2019, 8, 409. Choi, M.-J.; Kang, H.; Lee, Y.Y.; Choo, O.-S.; Jang, J.H.; Park, S.-H.; Moon, J.-S.; Choi, S.J.; Choung, Y.-H. Cisplatin-Induced Ototoxicity in Rats Is Driven by RIP3-Dependent Necroptosis. Cells 2019, 8, 409.

Journal reference: Cells 2019, 8, 409
DOI: 10.3390/cells8050409

Abstract

Cisplatin induces early-onset ototoxicity, resulting in hearing loss. The exact mechanism by which cisplatin causes ototoxicity remains unclear. The purpose of this study was to identify the involvement of receptor-interacting protein kinase(RIP)3-dependent necroptosis in cisplatin-induced ototoxicity in animal models. Sprague–Dawley rats (SD, 8 week) were treated via intraperitoneal (i.p) injection with cisplatin (16 mg/kg for 1 day), and their hearing thresholds were was measured by the auditory brainstem response (ABR) method. Hematoxylin and eosin (H-E) staining, immunohistochemistry, and western blots were performed to determine the effect of cisplatin-induced ototoxicity on cochlear morphology. H-E stains outlined necroptotic changes in the organ of Cortis (OCs) and spiral ganglion neurons (SGNs). Additionally, immunohistochemistry and western blot analysis showed overexpression of RIP3 in the OCs and SGNs that were treated with cisplatin. These results suggest that RIP3-dependent necroptosis was substantial in cisplatin-induced ototoxicity; inner cochlear regions, the OCs, and SGNs were especially sensitive to necroptosis.

Subject Areas

necroptosis; cisplatin; ototoxicity; organ of corti; spiral ganglion neuron

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