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Anisomycin induces hair cell death and blocks supporting cell proliferation in zebrafish lateral line neuromast
Xiaoyi Yuan1, Yanjun Qin1, Jian Wang2
1International Research Center for Marine Biosciences, Ministry of Science and Technology, Shanghai Ocean University, China; Institute for Marine Biosystem and Neuroscience, International Center for Marine Studies, Shanghai Ocean University, Shanghai, China.
Abstract:
Ototoxicity of drugs is an important inducement for hearing loss. Anisomycin is a candidate drug for parasite, cancer, immunosuppression, and mental disease. However, the ototoxicity of anisomycin has not been examined. In this study, the ototoxicity of anisomycin was evaluated using zebrafish lateral line. We found the zebrafish treated with anisomycin during lateral line development could inhibit hair cell formation in a time- and dose-dependent manner. After neuromasts are mature with differentiated hair cells by 5 day post-fertilization, anisomycin could induce hair cell loss effectively through chronic exposure rather than acute exposure. TUNEL assay and qPCR of apoptosis related genes tp53, casp8, casp3a, and casp3b indicated that cell apoptotic was induced by chronic anisomycin exposure. Furthermore, knocking down tp53 with antisense morpholino could attenuate the hair cell loss induced by anisomycin. In addition, we found that anisomycin chronic exposure also inhibited the proliferation of supporting cell. Together, these results indicate that chronic anisomycin exposure could induce hair cell death and block supporting cell proliferation, which causes hair cell loss in zebrafish neuromast. This study provides primary ototoxicity evaluation for anisomycin.
Insights
Anisomycin, a potential drug, causes hearing loss by damaging hair cells in zebrafish. Chronic exposure induces hair cell death and inhibits supporting cell proliferation, highlighting its ototoxicity.
Area of Science:
- Ototoxicity and Drug Development
- Zebrafish as a Model Organism
- Cell Biology and Apoptosis
Background:
- Drug-induced ototoxicity is a significant cause of hearing loss.
- Anisomycin is being investigated for various therapeutic applications.
- The ototoxic potential of anisomycin remains unexamined.
Purpose of the Study:
- To evaluate the ototoxicity of anisomycin.
- To investigate the mechanism of anisomycin-induced hair cell damage.
- To provide an initial ototoxicity assessment for anisomycin.
Main Methods:
- Utilized zebrafish lateral line to assess ototoxicity.
- Examined anisomycin effects on hair cell formation and loss.
- Employed TUNEL assay and qPCR to analyze apoptosis.
- Investigated the role of tp53 in anisomycin-induced ototoxicity.
- Assessed the impact on supporting cell proliferation.
Main Results:
- Anisomycin inhibited hair cell formation in a time- and dose-dependent manner.
- Chronic anisomycin exposure induced hair cell loss, while acute exposure did not.
- Apoptosis, involving tp53, casp8, casp3a, and casp3b, was induced by chronic exposure.
- Knocking down tp53 partially rescued anisomycin-induced hair cell loss.
- Anisomycin inhibited supporting cell proliferation.
Conclusions:
- Chronic anisomycin exposure leads to hair cell death and loss via apoptosis.
- Anisomycin also inhibits supporting cell proliferation, contributing to hair cell loss.
- This study establishes the ototoxicity of anisomycin using a zebrafish model.
