Downregulation of Protein Kinase C Isozymes on Cholesteatoma.
- Author:
Nam Pyo HONG
1
;
Chang Sik PARK
;
Young Ho SONG
;
Jae Yong BYUN
;
Hwoe Young AHN
;
Chang Il CHA
Author Information
1. Department of Otolaryngology, College of Medicine, Kyung Hee University, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Signal transduction;
Cholesteatoma;
Downregulation;
Protein kinase C(PKC) isoenzyme;
Post-trans-cription
- MeSH:
Blotting, Western;
Cholesteatoma*;
Densitometry;
Down-Regulation*;
Epithelial Cells;
Humans;
Inflammation;
Polymerase Chain Reaction;
Protein Kinase C*;
Protein Kinases*;
RNA, Messenger;
Signal Transduction;
Skin
- From:Korean Journal of Otolaryngology - Head and Neck Surgery
1998;41(6):685-695
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND AND OBJECTIVES: The exact pathogenesis of cholesteatoma remains unknown in spite of several theories that have been formulated. The most characteristic histologic finding of cholesteatoma is the proliferation of the squamous cell lining of the lesion. Protein Kinase C (PKC) is a family of phospholipid-dependent serine/threonin protein kinase that sends extracellular signals across the cell surface in order to regulate epithelial cell groweth and differentiation. This study attempted to provide the evidence for the role of PKC in cholesteatoma. MATERIALS AND METHODS: Twenty-five cholesteatoma specimens were obtained from patients for western blotting, immunohistochemical study, RT-PCR, and densitometry. RESULTS: The results of western blotting revealed that considerably lower levels of PKCalpha, PKCbeta, and PKCepsilon protein were detected in cholesteatoma than in the posterior auricular skin. In the immunohistochemical study, PKCalpha, PKCbeta, and PKCepsilon were detected both in the basal and suprabasal layer of posterior auricular skin, but they were not detectable in cholesteatoma. The results of PCR for PKCalpha, PKCbeta, and PKCepsilon showed that there were no differences between cholesteatoma and posterior auricular skin regarding the mRNA expression. CONCLUSION: Downregulation of PKCalpha, PKCbeta, and PKCepsilon in cholesteatoma suggests that abnormal epithelial growth is a possible mechanism of cholesteatoma. The results suggest the following there is an abnormal signal transduction through the PKC pathway in cholesteatoma: downregulation of PKC takes place in the post-transcription phase, and downregulation of PKC is associated with prolonged chronic inflammation of cholesteatoma.
