Pcolce2 overexpression promotes supporting cell reprogramming in the neonatal mouse cochlea.
Cell Prolif
; 57(8): e13633, 2024 Aug.
Article
in En
| MEDLINE
| ID: mdl-38528645
ABSTRACT
Hair cell (HC) damage is a leading cause of sensorineural hearing loss, and in mammals supporting cells (SCs) are unable to divide and regenerate HCs after birth spontaneously. Procollagen C-endopeptidase enhancer 2 (Pcolce2), which encodes a glycoprotein that acts as a functional procollagen C protease enhancer, was screened as a candidate regulator of SC plasticity in our previous study. In the current study, we used adeno-associated virus (AAV)-ie (a newly developed adeno-associated virus that targets SCs) to overexpress Pcolce2 in SCs. AAV-Pcolce2 facilitated SC re-entry into the cell cycle both in cultured cochlear organoids and in the postnatal cochlea. In the neomycin-damaged model, regenerated HCs were detected after overexpression of Pcolce2, and these were derived from SCs that had re-entered the cell cycle. These findings reveal that Pcolce2 may serve as a therapeutic target for the regeneration of HCs to treat hearing loss.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Cochlea
/
Cellular Reprogramming
/
Animals, Newborn
Limits:
Animals
Language:
En
Journal:
Cell Prolif
Year:
2024
Type:
Article
Affiliation country:
China