EXPRESSION AND LOCALIZATION OF MESSENGER-RNA FOR EPIDERMAL GROWTH-FACTOR AND EPIDERMAL GROWTH-FACTOR RECEPTOR IN HUMAN CHOLESTEATOMA
EXPRESSION AND LOCALIZATION OF MESSENGER-RNA FOR EPIDERMAL GROWTH-FACTOR AND EPIDERMAL GROWTH-FACTOR RECEPTOR IN HUMAN CHOLESTEATOMA
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DOI：
10.3109/00016489409126081
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发表时间：
1994-07-01
影响因子：
1.4
通讯作者：
MORIYAMA, H
中科院分区：
文献类型：
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作者：
KOJIMA, H;SHIWA, M;MORIYAMA, H
本文研究了表皮生长因子（EGF）及其受体（EGF-R）在中耳乳突瘤上皮增殖和发展中的作用。本文应用非放射性原位杂交技术，探讨了表皮生长因子（EGF）mRNA和内皮细胞生长因子受体（ECF-R）mRNA在中耳乳突瘤上皮中的定位和程度。在这项研究中使用了10例手术切除的中耳乳突瘤标本和6例从外耳道收集的正常皮肤标本（对照）。6个对照标本中只有1个标本的部分基底细胞中有EGF mRNA信号轻度表达，而10个标本中有5个标本的胆脂瘤上皮基底细胞中有沿着强烈表达。EGF-R mRNA的信号沿着基底细胞层观察到在6个对照标本中的5个，而信号强烈表达在所有10个标本中的所有层的中耳炎上皮细胞。在基底细胞层表达尤为明显。这些结果表明，在几乎整个上皮层的中耳炎的EGF-R mRNA的异常表达的可能性是由于EGF-R基因的过度表达，并有一个机制，上皮基底细胞增殖通过自分泌调节系统通过EGF和EGF-R。
The roles of epidermal growth factor (EGF) and epidermal growth factor receptor (EGF-R) in the proliferation and progression of the epithelium of middle ear cholesteatoma were studied. An attempt was made to elucidate the site and degree of localization of the EGF mRNA and ECF-R mRNA in the epithelium of the cholesteatoma by means of the non-radioactive in situ hybridization method. Ten cholesteatoma specimens excised during operations and six normal skin specimens (control) collected from the external ear canal were used in this study. The signal of the EGF mRNA was slightly expressed in part of the basal cells in only one of the six control specimens, while the signal was strongly expressed along the basal cells of the cholesteatoma epithelium in five of the ten specimens. The signal of the EGF-R mRNA was observed along the basal cell layer in five of the six control specimens, while the signal was strongly expressed in all layers of the cholesteatoma epithelium in all ten specimens. The expression was especially marked in the basal cell layer. These findings suggest the possibilities that abnormal expression of the EGF-R mRNA in nearly entire epithelial layers of cholesteatoma is due to overexpression of EGF-R gene, and that there is a mechanism of epithelial basal cell proliferation through an autocrine regulatory system via EGF and EGF-R.