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Author Notes:

Correspondence: Dong-dong Ren, dongdongren@fudan.edu.cn Juan-mei Yang, yangjuanmei1982@126.com

WL, DR, PC, FC, and JY: Designed the experiments; WL, XW, RM, NC, and YG: Performed the experiments; WL and JY: Wrote and revised the paper; PC, FC, DR, NC, and JY: Provided financial support for the project.

We would like to thank Pro. Chai Renjie (Southeast University) to help us revise and polish the paper.

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Subjects:

Research Funding:

This study was supported by the National Natural Science Foundation of China (NSFC) Grant NO. 81420108010, FC, Key Project of Chinese National Programs (2016YFC0905200, 2016YFC0905202).

The Innovation Project of Shanghai Municipal Science and Technology Commission (grant no. 11411952300) to FC.

Additional support was provided by Grants 81200740 to JY, 81771077, 81370022, 81570920, 81000413 to DR, and 81200738 to NC and the Innovation Project of Shanghai Municipal Science and Technology Commission (Grant No. 11411952300) to FC.

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Neurosciences
  • Neurosciences & Neurology
  • cochlea
  • supporting cells
  • hair cells
  • SC-to-HC conversion
  • DAPT
  • E-cadherin/p120ctn complexes
  • MAMMALIAN INNER-EAR
  • NEONATAL MOUSE COCHLEA
  • E-CADHERIN
  • IN-VIVO
  • ACOUSTIC TRAUMA
  • INTERCELLULAR-JUNCTIONS
  • P120 CATENIN
  • REGENERATION
  • PROLIFERATION
  • NOTCH

Junctional E-cadherin/p120-catenin Is Correlated with the Absence of Supporting Cells to Hair Cells Conversion in Postnatal Mice Cochleae

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Journal Title:

Frontiers in Molecular Neuroscience

Volume:

Volume 11

Publisher:

, Pages 20-20

Type of Work:

Article | Final Publisher PDF

Abstract:

Notch inhibition is known to generate supernumerary hair cells (HCs) at the expense of supporting cells (SCs) in the mammalian inner ear. However, inhibition of Notch activity becomes progressively less effective at inducing SC-to-HC conversion in the postnatal cochlea and balance organs as the animal ages. It has been suggested that the SC-to-HC conversion capacity is inversely correlated with E-cadherin accumulation in postnatal mammalian utricles. However, whether E-cadherin localization is linked to the SC-to-HC conversion capacity in the mammalian inner ear is poorly understood. In the present study, we treated cochleae from postnatal day 0 (P0) with the Notch signaling inhibitor DAPT and observed apparent SC-to-HC conversion along with E-cadherin/p120ctn disruption in the sensory region. In addition, the SC-to-HC conversion capacity and E-cadherin/p120ctn disorganization were robust in the apex but decreased toward the base. We further demonstrated that the ability to regenerate HCs and the disruption of E-cadherin/p120ctn concomitantly decreased with age and ceased at P7, even after extended DAPT treatments. This timing is consistent with E-cadherin/p120ctn accumulation in the postnatal cochleae. These results suggest that the decreasing capacity of SCs to transdifferentiate into HCs correlates with E-cadherin/p120ctn localization in the postnatal cochleae, which might account for the absence of SC-to-HC conversion in the mammalian cochlea.

Copyright information:

© 2018 Luo, Wang, Ma, Chi, Chen, Cong, Gu, Ren and Yang.

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