Cisplatin-induced ototoxicity in organotypic cochlear cultures occurs independent of gap junctional intercellular communication.

ABSTRACT: Cisplatin is a very effective chemotherapeutic, but severe and permanent hearing loss remains a prevalent side effect. The processes underpinning cisplatin-induced ototoxicity are not well understood. Gap junction channels composed of connexin (Cx) subunits allow for the passage of small molecules and ions between contacting neighboring cells. These specialized channels have been postulated to enhance cisplatin-induced cell death by spreading "death signals" throughout the supporting cells of the organ of Corti. This study sought to investigate the role of Cx43 in cisplatin-induced ototoxicity using organotypic cochlear cultures from control and two Cx43-mutant mouse strains harboring either a moderate (Cx43^I130T/+) or severe (Cx43^G60S/+) reduction of Cx43 function. C

SUBMITTER: Abitbol J 

PROVIDER: S-EPMC7214471 | biostudies-literature | 2020 May

REPOSITORIES: biostudies-literature