MicroRNA-222 alleviates radiation-induced apoptosis by targeting BCL2L11 in cochlea hair cells.

Yan-Yan Zhang,Gao-Yun Xiong,Xiao-Xing Xie

doi:10.1042/bsr20201397

Yan-Yan Zhang, Gao-Yun Xiong + Show 1 more

Open Access

https://doi.org/10.1042/bsr20201397

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Journal: Bioscience reports	Publication Date: Jun 4, 2021
Citations: 2	License type: CC BY 4.0

Affiliation: Tongde Hospital of Zhejiang Province

Abstract

Radiation-induced hair cell injury is detrimental for human health but the underlying mechanism is not clear. MicroRNAs (miRNAs) have critical roles in various types of cellular biological processes. The present study investigated the role of miR-222 in the regulation of ionizing radiation (IR)-induced cell injury in auditory cells and its underlying mechanism. Real-time PCR was performed to identify the expression profile of miR-222 in the cochlea hair cell line HEI-OC1 after IR exposure. miRNA mimics or inhibitor-mediated up- or down-regulation of indicated miRNA was applied to characterize the biological effects of miR-222 using MTT, apoptosis and DNA damage assay. Bioinformatics analyses and luciferase reporter assays were applied to identify an miRNA target gene. Our study confirmed that IR treatment significantly suppressed miR-222 levels in a dose-dependent manner. Up-regulation of miR-222 enhances cell viability and alleviated IR-induced apoptosis and DNA damage in HEI-OC1 cells. In addition, BCL-2-like protein 11 (BCL2L11) was validated as a direct target of miR-222. Overexpression of BCL2L11 abolished the protective effects of miR-222 in IR-treated HEI-OC1 cells. Moreover, miR-222 alleviated IR-induced apoptosis and DNA damage by directly targeting BCL2L11. The present study demonstrates that miR-222 exhibits protective effects against irradiation-induced cell injury by directly targeting BCL2L11 in cochlear cells.

Highlights

Hearing impairment is detrimental for human health, affecting communication and impacting quality of life
Another study investigated the functions of miR-207 in the regulation of ionizing radiation (IR)-induced cell death in auditory cells; their findings suggested that miR-207 promoted radiation-induced apoptosis by directly targeting Akt3 in cochlea hair cells [8]
IR exposure led to a dose-dependent up-regulation of miR-222 in HEI-OC1 cells, suggesting that miR-222 may be involved in auditory pathway

Summary

Introduction

Hearing impairment is detrimental for human health, affecting communication and impacting quality of life. Hearing impairment induced by radiation therapy, such as sensorineural hearing loss (SNHL), is a common complication following radiotherapy [2,3]. MicroRNAs (miRNAs) are a group of small, noncoding RNAs. By post-transcriptional regulation of target mRNAs through complementary binding to the 3 untranslated region (UTR), they play diverse roles in cellular behaviors, including cell proliferation, apoptosis, differentiation, and angiogenesis [4]. The specific role of miRNAs in radiation-induced cochlea hair cell injury is limited [6]. Another study investigated the functions of miR-207 in the regulation of ionizing radiation (IR)-induced cell death in auditory cells; their findings suggested that miR-207 promoted radiation-induced apoptosis by directly targeting Akt in cochlea hair cells [8]

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