Takahashi Satoe, Homma Kazuaki, Zhou Yingjie, Nishimura Shinichi, Duan Chongwen, Chen Jessie, Ahmad Aisha, Cheatham Mary Ann, Zheng Jing
Department of Otolaryngology - Head and Neck Surgery, Feinberg School of Medicine, Northwestern University, Chicago IL 60611, USA.
Knowles Hearing Center, Northwestern University, Evanston, IL 60208, USA.
Sci Rep. 2016 Feb 23;6:21973. doi: 10.1038/srep21973.
Niemann-Pick type C1 disease (NPC1) is a fatal genetic disorder caused by impaired intracellular cholesterol trafficking. Recent studies reported ototoxicity of 2-hydroxypropyl- β-cyclodextrin (HPβCD), a cholesterol chelator and the only promising treatment for NPC1. Because outer hair cells (OHCs) are the only cochlear cells affected by HPβCD, we investigated whether prestin, an OHC-specific motor protein, might be involved. Single, high-dose administration of HPβCD resulted in OHC death in prestin wildtype (WT) mice whereas OHCs were largely spared in prestin knockout (KO) mice in the basal region, implicating prestin's involvement in ototoxicity of HPβCD. We found that prestin can interact with cholesterol in vitro, suggesting that HPβCD-induced ototoxicity may involve disruption of this interaction. Time-lapse analysis revealed that OHCs isolated from WT animals rapidly deteriorated upon HPβCD treatment while those from prestin-KOs tolerated the same regimen. These results suggest that a prestin-dependent mechanism contributes to HPβCD ototoxicity.
尼曼-匹克C1型病(NPC1)是一种由细胞内胆固醇转运受损引起的致命性遗传疾病。最近的研究报道了2-羟丙基-β-环糊精(HPβCD)的耳毒性,HPβCD是一种胆固醇螯合剂,也是目前唯一有希望治疗NPC1的药物。由于外毛细胞(OHC)是受HPβCD影响的唯一耳蜗细胞,我们研究了OHC特异性运动蛋白prestin是否与之有关。单次高剂量给予HPβCD导致prestin野生型(WT)小鼠的OHC死亡,而在prestin基因敲除(KO)小鼠的基底区域,OHC在很大程度上得以幸免,这表明prestin参与了HPβCD的耳毒性作用。我们发现prestin在体外可与胆固醇相互作用,提示HPβCD诱导的耳毒性可能涉及这种相互作用的破坏。延时分析显示,来自WT动物的OHC在HPβCD处理后迅速恶化,而来自prestin-KO小鼠的OHC对相同处理有耐受性。这些结果表明,一种依赖prestin的机制导致了HPβCD的耳毒性。