Expression of Caveolin-1 in the Differentiated Vestibular Cell Line (UB/UE-1) after Gentamicin Toxicity.
- Author:
Byung Han CHO
1
;
Kyu Sung KIM
;
Min Wook KIM
;
Min Sun KIM
;
Byung Rim PARK
Author Information
1. Department of Otolaryngology-Head & Neck Surgery, Inha University College of Medicine, Incheon, Korea. stedman@inha.ac.kr
- Publication Type:Original Article
- Keywords:
Caveolin;
Gentamicin;
Ototoxicity
- MeSH:
Animals;
Blotting, Western;
Caveolae;
Caveolin 1*;
Cell Death;
Cell Line*;
Gentamicins*;
Guinea Pigs;
Hair Cells, Vestibular;
Mice;
Protein Kinases
- From:Journal of the Korean Balance Society
2005;4(2):243-249
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND AND OBJECTIVES: The caveolin is known as a mediator of cell death or survival of injured cell and inhibitor of various signaling pathways. We examined expression of caveolin-1 involved by protein kinase A(PKA) signaling pathway in the differentiated mouse vestibular cell line(UB/UE-1) after gentamicin toxicity. MATERIALS AND METHOD: We observed caveolae in the vestibular hair cell of healthy guinea pig through electron microscope. UB/UE-1 cells were cultured at 95% CO2, 5% O2, 33DegreeC for 2days and at 95% CO2, 5% O2, 39DegreeC for 24 hours for differentiation. Cells were treated with 1 mM of gentamicin, 0.02 mM H89 (PKA inhibitor), and then incubated for 24 hours. Caveolin-1 expression was examined by western blot and PKA activity by PepTag? assay. RESULTS: Caveolae were observed in the vestibular hair cell of healthy guinea pig by electron microscope. Caveolin-1 was expressed spontaneously in differentiated UB/UE-1 cells and increased after gentamicin treatment. PKA is overactivated by gentamicin treatment. The gentamicin induced caveolin-1 expression and PKA overactivation was inhibited by H89. CONCLUSION: Our results indicate that gentamicin induced caveolin-1 expression is mediated by PKA signaling pathway. We conclude that the caveolae/caveolin through a PKA signaling pathway is the important mechanism of gentamicin induced ototoxicity.
