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Gap junction-mediated intercellular communication of cAMP prevents CDDP-induced ototoxicity via cAMP/PKA/CREB pathway

Authors
Kim, YJ  | Lee, JS | Kim, H  | Jang, JH  | Choung, YH
Citation
International journal of molecular sciences, 22(12). : 6327-6327, 2021
Journal Title
International journal of molecular sciences
ISSN
1661-65961422-0067
Abstract
In the cochlea, non-sensory supporting cells are directly connected to adjacent supporting cells via gap junctions that allow the exchange of small molecules. We have previously shown that the pharmacological regulation of gap junctions alleviates cisplatin (CDDP)-induced ototoxicity in animal models. In this study, we aimed to identify specific small molecules that pass through gap junctions in the process of CDDP-induced auditory cell death and suggest new mechanisms to prevent hearing loss. We found that the cyclic adenosine monophosphate (cAMP) inducer forskolin (FSK) significantly attenuated CDDP-induced auditory cell death in vitro and ex vivo. The activation of cAMP/PKA/CREB signaling was observed in organ of Corti primary cells treated with FSK, especially in supporting cells. Co-treatment with gap junction enhancers such as all-trans retinoic acid (ATRA) and quinoline showed potentiating effects with FSK on cell survival via activation of cAMP/PKA/CREB. In vivo, the combination of FSK and ATRA was more effective for preventing ototoxicity compared to either single treatment. Our study provides the new insight that gap junction-mediated intercellular communication of cAMP may prevent CDDP-induced ototoxicity.
Keywords

MeSH

DOI
10.3390/ijms22126327
PMID
34199197
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Otolaryngology
Ajou Authors
김, 연주  |  김, 한태  |  장, 정훈  |  정, 연훈
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