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小鼠耳蜗衰老的单细胞转录组图谱。

Single-cell transcriptomic atlas of mouse cochlear aging.

机构信息

State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, China.

University of Chinese Academy of Sciences, Beijing 100049, China.

出版信息

Protein Cell. 2023 Apr 13;14(3):180-201. doi: 10.1093/procel/pwac058.

Abstract

Progressive functional deterioration in the cochlea is associated with age-related hearing loss (ARHL). However, the cellular and molecular basis underlying cochlear aging remains largely unknown. Here, we established a dynamic single-cell transcriptomic landscape of mouse cochlear aging, in which we characterized aging-associated transcriptomic changes in 27 different cochlear cell types across five different time points. Overall, our analysis pinpoints loss of proteostasis and elevated apoptosis as the hallmark features of cochlear aging, highlights unexpected age-related transcriptional fluctuations in intermediate cells localized in the stria vascularis (SV) and demonstrates that upregulation of endoplasmic reticulum (ER) chaperon protein HSP90AA1 mitigates ER stress-induced damages associated with aging. Our work suggests that targeting unfolded protein response pathways may help alleviate aging-related SV atrophy and hence delay the progression of ARHL.

摘要

耳蜗的功能进行性恶化与年龄相关性听力损失(ARHL)有关。然而,耳蜗老化的细胞和分子基础在很大程度上仍然未知。在这里,我们建立了一个小鼠耳蜗老化的动态单细胞转录组图谱,在其中我们描述了五个不同时间点的 27 种不同耳蜗细胞类型中与衰老相关的转录组变化。总的来说,我们的分析确定了蛋白质稳态的丧失和凋亡的升高是耳蜗老化的标志性特征,突出了位于血管纹(SV)中的中间细胞中意想不到的与年龄相关的转录波动,并表明内质网(ER)伴侣蛋白 HSP90AA1 的上调减轻了与衰老相关的 ER 应激诱导的损伤。我们的工作表明,靶向未折叠蛋白反应途径可能有助于减轻与衰老相关的 SV 萎缩,从而延缓 ARHL 的进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b37/10098046/b5ead5f439f1/pwac058f0001.jpg

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