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Cisplatin-Induced Ototoxicity in Rats Is Driven by RIP3-Dependent Necroptosis

Mi-Jin Choi1,2, Hyunsook Kang3, Yun Yeong Lee4,5

  • 1Department of Otolaryngology, Ajou University School of Medicine, Suwon 16499, Korea. cmjpink@naver.com.

Cells
|May 5, 2019
PubMed

Insights

Cisplatin causes hearing loss through receptor-interacting protein kinase 3 (RIPK3)-dependent necroptosis. This programmed cell death pathway significantly impacts the organ of Corti and spiral ganglion neurons, contributing to ototoxicity.

Area of Science:

  • Ototoxicity research
  • Cellular mechanisms of hearing loss
  • Necroptosis signaling pathways

Background:

  • Cisplatin is a common chemotherapy agent.
  • Cisplatin-induced ototoxicity leads to hearing loss.
  • The precise mechanisms underlying cisplatin ototoxicity are not fully understood.

Purpose of the Study:

  • To investigate the role of receptor-interacting protein kinase 3 (RIPK3)-dependent necroptosis in cisplatin-induced ototoxicity.
  • To elucidate the cellular and molecular pathways involved in cisplatin-induced damage to the cochlea.

Main Methods:

  • In vivo studies using Sprague-Dawley rats treated with cisplatin.
  • Auditory brainstem response (ABR) testing to measure hearing thresholds.
  • Histological analyses (H&E staining, immunohistochemistry) and Western blot to assess cochlear damage and protein expression.
  • In vitro experiments using HEI-OC1 cells treated with necrostatin-1 (Nec-1) and Z-VAD.

Main Results:

  • Cisplatin treatment increased necroptotic changes in the organ of Corti (OC) and spiral ganglion neurons (SGNs).
  • Cisplatin elevated RIPK3 protein levels in the OC and SGNs.
  • Necrostatin-1 (Nec-1) significantly suppressed cisplatin-induced cell death in HEI-OC1 cells, while Z-VAD did not.

Conclusions:

  • Receptor-interacting protein kinase 3 (RIPK3)-dependent necroptosis plays a substantial role in cisplatin-induced ototoxicity.
  • Inner cochlear structures, specifically the organ of Corti (OC) and spiral ganglion neurons (SGNs), are highly susceptible to necroptosis induced by cisplatin.
Keywords:
cisplatinnecroptosisorgan of Cortiototoxicityspiral ganglion neuron

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