Bhlhe40 protects cochlear hair cell-like HEI-OC1 cells against H_(2)O_(2) ‑triggered oxidative injury
作者机构:Department of OtorhinolaryngologyLonggang Otorhinolaryngology Hospital and Shenzhen Key Laboratory of OtorhinolaryngologyShenzhen Institute of OtorhinolaryngologyShenzhenChina
出 版 物:《BIOCELL》 (生物细胞(英文))
年 卷 期:2024年第48卷第6期
页 面:991-999页
核心收录:
学科分类:1002[医学-临床医学] 100213[医学-耳鼻咽喉科学] 10[医学]
基 金:This research was supported by the Special Fund for Economic and Technological Development of Longgang District Shenzhen(LGKCYLWS2021000030)
主 题:Bhlhe40 Oxidative injury Cochlear hair cell Histone deacetylases 2
摘 要:Background:Cochlear hair cell injury is a common pathological feature of hearing *** basic helix-loop-helix family,member e40(Bhlhe40),a gene belonging to the basic helix-loop-helix(bHLH)family,exhibits strong transcriptional repression ***:Oxidative damage,in House Ear Institute-Organ of Corti 1(HEI-OC1)cells,was caused using hydrogen peroxide(H2O2).The Ad-Bhlhe40 particles were constructed to overexpress Bhlhe40 in HEI-OC1 *** assays including cell counting kit-8(CCK-8),terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling assay(TUNEL),flow cytometry,immunofluorescence,and corresponding commercial kits were employed to investigate the impacts of Bhlhe40 on cell viability,apoptosis,oxidative stress levels,mitochondrial membrane potential and cellular ***,a dual-luciferase reporter assay was performed to confirm the targeting of the histone deacetylases 2(Hdac2)by ***:The results revealed that Bhlhe40 was downregulated in H_(2)O_(2)-treated HEI-OC1 cells,but its overexpression improved cell viability and mitigated H_(2)O_(2)-induced oxidative injury in HEI-OC1 cells with increase of superoxide dismutase(SOD),catalase(CAT)and glutathione peroxidase(GPx)activities and decrease of reactive oxygen species(ROS)***,overexpression of Bhlhe40 suppressed H_(2)O_(2)-triggered cell senescence,as evidenced by the fact that the upregulation of P53,P21,and P16 in HEI-OC1 cells treated with H2O2 were all alleviated by Bhlhe40 *** we further verified that overexpression of Bhlhe40 could inhibit the expression of Hdac2,which may be related to the repression of Hdac2 ***:This study suggests that Bhlhe40 plays a protective role against senescence and oxidative damage in cochlear hair cells exposed to H2O2.