Evidence map›Paper›PMID 38740884›Full record

ArticleScientific reports2024

Suppression of the TGF-β signaling exacerbates degeneration of auditory neurons in kanamycin-induced ototoxicity in mice.

Yoshihiro Nitta, Takaomi Kurioka, Sachiyo Mogi, Hajime Sano, Taku Yamashita

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PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

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0cells of the map it votes in
2citing papers in PubMed
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2 · The registry

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3 · Its place in the literature

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2 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Yoshihiro NittaDepartment of Otorhinolaryngology and Head and Neck Surgery, Kitasato University School of Medicine, 1-15-1 Kitasato, Minami-ku, Sagamihara, Kanagawa, 252-0374, Japan. n-yoshihiro@med.kitasato-u.ac.jp.
Takaomi KuriokaDepartment of Otorhinolaryngology, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama, 359-8513, Japan. takaomi@xj9.so-net.ne.jp.
Sachiyo MogiDepartment of Otorhinolaryngology and Head and Neck Surgery, Kitasato University School of Medicine, 1-15-1 Kitasato, Minami-ku, Sagamihara, Kanagawa, 252-0374, Japan.
Hajime SanoSchool of Allied Health Sciences, Kitasato University, Kanagawa, Japan.
Taku YamashitaDepartment of Otorhinolaryngology and Head and Neck Surgery, Kitasato University School of Medicine, 1-15-1 Kitasato, Minami-ku, Sagamihara, Kanagawa, 252-0374, Japan.

Funding

JSPS KAKENHI grant 23K15901
6 · The paper itself

Abstract

Transforming growth factor-β (TGF-β) signaling plays a significant role in multiple biological processes, including inflammation, immunity, and cell death. However, its specific impact on the cochlea remains unclear. In this study, we aimed to investigate the effects of TGF-β signaling suppression on auditory function and cochlear pathology in mice with kanamycin-induced ototoxicity. Kanamycin and furosemide (KM-FS) were systemically administered to 8-week-old C57/BL6 mice, followed by immediate topical application of a TGF-β receptor inhibitor (TGF-βRI) onto the round window membrane. Results showed significant TGF-β receptor upregulation in spiral ganglion neurons (SGNs) after KM-FA ototoxicity, whereas expression levels in the TGF-βRI treated group remained unchanged. Interestingly, despite no significant change in cochlear TGF-β expression after KM-FS ototoxicity, TGF-βRI treatment resulted in a significant decrease in TGF-β signaling. Regarding auditory function, TGF-βRI treatment offered no therapeutic effects on hearing thresholds and hair cell survival following KM-FS ototoxicity. However, SGN loss and macrophage infiltration were significantly increased with TGF-βRI treatment. These results imply that inhibition of TGF-β signaling after KM-FS ototoxicity promotes cochlear inflammation and SGN degeneration.

Indexed as

KanamycinOtotoxicitySignal TransductionTransforming Growth Factor betaAnimalsCochleaFurosemideHair Cells, AuditoryMiceMice, Inbred C57BLSpiral GanglionFurosemideKanamycinTransforming Growth Factor betaCochlear inflammationKanamycinOtotoxicitySpiral ganglion neuronTransforming growth factor-β

Identifiers

PMID38740884
PMCPMC11091189

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.