PTKs CDK4及p15在中耳胆脂瘤上皮的表达

Expression of PTKs CDK4 and p15 in the middle ear cholesteatomatous epithelium

目的 :从蛋白酪氨酸激酶 (PTKs)信号传递系统及细胞周期调控探讨胆脂瘤上皮细胞增殖的分子机制。方法 :采用免疫组织化学S P方法和计算机图像分析系统 ,观测 30例中耳胆脂瘤上皮及 19例胆脂瘤患者外耳道皮肤中磷酸化PTKs、周期蛋白依赖性激酶 4 (CDK4 )、p15的表达 ,并结合上皮下炎症浸润、骨质破坏程度作统计学分析。结果 :磷酸化PTKs以胞膜表达为主 ,CDK4胞核、胞质均有表达 ,以胞核为主 ,而p15仅以胞核表达。与外耳道皮肤相比 ,胆脂瘤上皮细胞磷酸化PTKs、CDK4、p15表达都显著增强 (P <0 .0 1) ,在重度皮下炎性浸润的上皮细胞磷酸化PTKs、CDK4表达增强 (P <0 .0 1) ;处于高水平磷酸化PTKs表达的胆脂瘤上皮细胞CDK4表达增强 (P <0 .0 1) ;两种骨质破坏程度中上述指标表达的差异无统计学意义 (P >0 .0 5 )。结论 :胆脂瘤上皮细胞具有过度增殖能力 ,同时也存在抑制细胞增殖的机制 ;

Objective:To explore the cells proliferation and its molecular regulating mechanisms of cholesteatomatous epithelium from the aspect of protein tyrosine kinases (PTKs) signal transduction and cell cycle control.Method:The expressions of phosphated PTKs, CDK4 and p15 were investigated by immunohistochemical S-P method and computer image analysis in 30 specimens of the middle ear cholesteatomatous epithelium and 19 specimens of external auditory canal epithelium from patients with chronic otitis media with cholesteatoma.The expressive results of phosphated PTKs,CDK4 and p15 were determined in same epithelium of different slices of same specimen.Statistical analysis was performed by the connection with degree of subepidermal inflammatory cell infiltration and degree of bone destruction.Result:The expression of phosphated PTKs was primarily staining in cell membrane,and the staining of CDK4 were located in the nuclei as well as the cytoplasm of cells,and the staining of nuclei was primary, but the staining of p15 was expressed only in the nuclei of cell.The expressions of phosphated PTKs,CDK4 and p15 in epithelium were clearly increased compared with that of external auditory canal epithelium(P< 0.01).The expression of phosphated PTKs and CDK4 tended to be strong in the epithelium with subepidermal inflammatory, and the expression of CDK4 tended to be strong in the epithelium with hight level expression of phosphated PTKs(P< 0.01).The expressions of above investigated indexes were not significantly different under the different degree of bone destruction(P> 0.05).Conclusion:The cholesteatomatous epithelium have a hyperproliferation ability,and also show a mechanism of inhibiting proliferation ability.The microenvironment with inflammatory cell infiltration has a tendency to greatly affect proliferation ability of cholesteatomatous epithelium.