Sun Wenzhong, Xu Zhiwen, Tang Anzhou, Su Jiping
Department of Otolaryngology, First Affiliated Hospital of Guangxi University of Medical Sciences, Nanning, 530021, China.
Lin Chuang Er Bi Yan Hou Ke Za Zhi. 2004 Oct;18(10):616-9.
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.
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.
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 high 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).
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.
从蛋白酪氨酸激酶（PTKs）信号转导及细胞周期调控方面探讨胆脂瘤上皮细胞增殖及其分子调控机制。
采用免疫组织化学S-P法及计算机图像分析技术，对30例慢性胆脂瘤型中耳炎患者的中耳胆脂瘤上皮标本及19例外耳道上皮标本，检测磷酸化PTKs、细胞周期蛋白依赖性激酶4（CDK4）及p15的表达。在同一标本不同切片的相同上皮中测定磷酸化PTKs、CDK4及p15的表达结果。并与表皮下炎性细胞浸润程度及骨质破坏程度进行相关性统计分析。
磷酸化PTKs主要在细胞膜呈阳性染色，CDK4在细胞核及细胞质均有表达，以细胞核为主，而p15仅在细胞核表达。胆脂瘤上皮中磷酸化PTKs、CDK4及p15的表达明显高于外耳道上皮（P<0.01）。表皮下有炎症的上皮中磷酸化PTKs及CDK4表达增强，磷酸化PTKs高表达的上皮中CDK4表达增强（P<0.01）。不同程度骨质破坏情况下上述检测指标表达差异无统计学意义（P>0.05）。
胆脂瘤上皮具有增殖亢进能力，也存在增殖抑制机制。炎性细胞浸润的微环境对胆脂瘤上皮增殖能力有较大影响倾向。
