Korean J Otolaryngol-Head Neck Surg.
2004 Oct;47(10):968-972.
Alteration in Expression of p27(Kip1) in Mouse Vestibular Epithelia during Apoptosis Induced by Gentamicin
- Affiliations
-
- 1Department of Otolaryngology-Head & Neck Surgery, College of Medicine, Kyungpook National University, Daegu, Korea. leeshu@knu.ac.kr
- 2Seoul Municipal Dongbu Hospital, Seoul, Korea.
Abstract
- BACKGROUND AND OBJECTIVES
p27(Kip1), a novel cyclin-dependent kinase inhibitor, plays a crucial role in regulation of cell proliferation during development of inner ear. In addition, p27(Kip1) is known to regulate cell death in avian auditory epithelia. However, only a little is known about its role in aminoglycoside-induced mammalian vestibular degeneration. The aim of this study was to examine roles of p27(Kip1) in gentamicin-induced vestibulotoxicity.
MATERIALS AND METHOD: C57BL/6J mice were used as experimental animals. Ampullar cristae damaged by local application of gentamicin were provided for histological analyses and western blotting. TUNEL assay was used to detect apoptosis. Immunohistochemistry and western blotting for p27(Kip1) were performed to investigate its expression.
RESULTS
TUNEL-positive cells were detected in the hair cells of gentamicin-treated mice. Expression of p27(Kip1) was found in the supporting cells, but not in the hair cells. Gentamicin treatment caused degeneration of vestibular hair cells, and a decrease of numbers of p27(Kip1)-positive cells. The western blotting showed that expression of p27(Kip1) was markedly decreased on day 3.
CONCLUSION
The present findings indicate that p27(Kip1) may play roles in repair of hair cells by regenerative proliferation or transdifferentiation of supporting cells, but not in cell death of hair cells.