Expression of Phospholipase C-beta1 and Phospholipase C-gamma1 on Cholesteatoma

Song, Young Ho; Hong, Nam Pyo; Lee, Dong Yeup; Kim, Young Doe; Ahn, Hwoe Young; Cha, Chang Il

Abstract

BACKGROUND AND OBJECTIVES: A histological finding that is the most characteristic of cholesteatoma is the proliferation of the squamous cell. Signal transduction through phospholipase C(PLC) participates in the regulation of epidermal cell growth and differentiation. EGF, PDGF, and TGF-alpha bind to their receptors and thereby induce tyrosine phosphorylation of the phospholipase C-gamma1 (PLC-gamma1). PLC-gamma1 is a substrate for several receptor tyrosine kinases and its catalytic activity is increased by tyrosine phosphorylation. Tyrosine kinase phosphorylation of PLC-gamma1 stimulates PLC activation and cell proliferation. The G-protein has been shown to specifically activate PLC-beta1. However, the signal transduction pathway and the significance of PLC in cholesteatoma is unknown. This study attempted to provide some evidence that PLC plays a role in cholesteatoma by investigating the distribution and quantity of PLC-beta1 and PLC-gamma1 in the posterior auricular skin and cholestsatoma.
MATERIALS AND METHODS
Western blotting and immunohistochemical study were performed for 20 cholesteatoma specimens obtained from patients who underwent operation.
RESULTS
Western blot analyses revealed that PLC-beta1 protein and PLC-gamma1 protein were detectable in cholesteatoma and that these proteins were in higher levels compared with the control. In the imm-unohistochemical study, PLC-gamma1 was detected in the horny cell layer of posterior auricular skin but not in the suprabasal layer and the horny cell layer of cholesteatoma. PLC-beta1 was detected in the primary basal layer and a minor reaction was also noted in the spinous layer of posterior auricular skin. However, there were detactable reactions in both the basal and the suprabasal layers of cholesteatoma.
CONCLUSION
The results of this study suggest that there are signal transduction pathways through PLC, over-expression of PLC, the different signaling mechanism by PLC in the basal and the suprabasal layer of cholesteatoma.