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PNAS:阻断Notch信号有望恢复听力

来源:生物谷 2014-12-30 09:41

2014年12月29日讯 /生物谷BIOON/ --感觉毛细胞缺失是听力损失和平衡障碍的主要原因。产后哺乳动物内耳祖细胞具有再生毛细胞和恢复听觉的潜能,但控制其增殖和毛细胞再生的机制仍有待确定。

科学家已经表明阻断Notch途径(已知能操控内耳复杂毛细胞的分布)在决定耳蜗祖细胞增殖能力中起着至关重要的作用。他们的研究成果发表在PNAS杂志上。

高水平Notch活性防止祖细胞分裂,以及产后内耳毛细胞的再生。已知的是抑制Notch活性可以转换内耳支持细胞为毛细胞。在本研究中,我们已经表明,Notch抑制还促进细胞分裂。在此条件下,内耳祖细胞重新进入细胞分裂,再在产后耳蜗中生成毛细胞。

这项研究从而提供了一种新的途径来阻止Notch活性,以增加祖细胞群分裂,并再生新的毛细胞。我们的工作可能导致开发新策略以实现毛细胞再生,恢复听力。(生物谷Bioon.com)

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Notch inhibition induces mitotically generated hair cells in mammalian cochleae via activating the Wnt pathway.

Wenyan Li, Jingfang Wu, Jianming Yang, Shan Sun, Renjie Chai, Zheng-Yi Chen, Huawei Li.

The activation of cochlear progenitor cells is a promising approach for hair cell (HC) regeneration and hearing recovery. The mechanisms underlying the initiation of proliferation of postnatal cochlear progenitor cells and their transdifferentiation to HCs remain to be determined. We show that Notch inhibition initiates proliferation of supporting cells (SCs) and mitotic regeneration of HCs in neonatal mouse cochlea in vivo and in vitro. Through lineage tracing, we identify that a majority of the proliferating SCs and mitotic-generated HCs induced by Notch inhibition are derived from the Wnt-responsive leucine-rich repeat-containing G protein-coupled receptor 5 (Lgr5+) progenitor cells. We demonstrate that Notch inhibition removes the brakes on the canonical Wnt signaling and promotes Lgr5+ progenitor cells to mitotically generate new HCs. Our study reveals a new function of Notch signaling in limiting proliferation and regeneration potential of postnatal cochlear progenitor cells, and provides a new route to regenerate HCs from progenitor cells by interrupting the interaction between the Notch and Wnt pathways.

 

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