Hippo/YAP signaling pathway protects against neomycin-induced hair cell damage in the mouse cochlea.
Aminoglycosides
Apoptosis
Hair cells
Hippo/YAP signaling pathway
Protection
Sensorineural hearing loss (SNHL)
Journal
Cellular and molecular life sciences : CMLS
ISSN: 1420-9071
Titre abrégé: Cell Mol Life Sci
Pays: Switzerland
ID NLM: 9705402
Informations de publication
Date de publication:
19 Jan 2022
19 Jan 2022
Historique:
received:
24
08
2021
accepted:
08
11
2021
revised:
23
10
2021
entrez:
19
1
2022
pubmed:
20
1
2022
medline:
27
1
2022
Statut:
epublish
Résumé
The Hippo/Yes-associated protein (YAP) signaling pathway has been shown to be able to maintain organ size and homeostasis by regulating cell proliferation, differentiation, and apoptosis. The abuse of aminoglycosides is one of the main causes of sensorineural hearing loss (SSNHL). However, the role of the Hippo/YAP signaling pathway in cochlear hair cell (HC) damage protection in the auditory field is still unclear. In this study, we used the YAP agonist XMU-MP-1 (XMU) and the inhibitor Verteporfin (VP) to regulate the Hippo/YAP signaling pathway in vitro. We showed that YAP overexpression reduced neomycin-induced HC loss, while downregulated YAP expression increased HC vulnerability after neomycin exposure in vitro. We next found that activation of YAP expression inhibited C-Abl-mediated cell apoptosis, which led to reduced HC loss. Many previous studies have reported that the level of reactive oxygen species (ROS) is significantly increased in cochlear HCs after neomycin exposure. In our study, we also found that YAP overexpression significantly decreased ROS accumulation, while downregulation of YAP expression increased ROS accumulation. In summary, our results demonstrate that the Hippo/YAP signaling pathway plays an important role in reducing HC injury and maintaining auditory function after aminoglycoside exposure. YAP overexpression could protect against neomycin-induced HC loss by inhibiting C-Abl-mediated cell apoptosis and decreasing ROS accumulation, suggesting that YAP could be a novel therapeutic target for aminoglycosides-induced sensorineural hearing loss in the clinic.
Identifiants
pubmed: 35044530
doi: 10.1007/s00018-021-04029-9
pii: 10.1007/s00018-021-04029-9
pmc: PMC8770373
doi:
Substances chimiques
Anti-Bacterial Agents
0
Protein Synthesis Inhibitors
0
YAP-Signaling Proteins
0
Yap1 protein, mouse
0
Neomycin
I16QD7X297
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
79Subventions
Organisme : the National Natural Science Foundation of China
ID : 81970884
Organisme : the National Natural Science Foundation of China
ID : 81900941
Organisme : the National Natural Science Foundation of China
ID : 81900944
Organisme : the National Natural Science Foundation of China
ID : 81622013
Organisme : the National Natural Science Foundation of China
ID : 81970882
Organisme : the National Natural Science Foundation of China
ID : 81570919
Organisme : the National Natural Science Foundation of China
ID : 81870721
Organisme : the National Natural Science Foundation of China
ID : 81771019
Organisme : the National Natural Science Foundation of China
ID : 81700913
Organisme : the National Natural Science Foundation of China
ID : 81670928
Organisme : the National Natural Science Foundation of China
ID : 81570921
Organisme : the National Key R&D Program of China
ID : 2017YFA0103903
Organisme : the Strategic Priority Research Program of the Chinese Academy of Science
ID : XDA16010303
Informations de copyright
© 2022. The Author(s).
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