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首页> 外文期刊>Virchows Archiv: an international journal of pathology >Proliferation and number of Clara cell 10-kDa protein (CC10)-reactive epithelial cells and basal cells in normal, hyperplastic and metaplastic bronchial mucosa.
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Proliferation and number of Clara cell 10-kDa protein (CC10)-reactive epithelial cells and basal cells in normal, hyperplastic and metaplastic bronchial mucosa.

机译:正常,增生和化生支气管黏膜中Clara细胞10-kDa蛋白(CC10)反应性上皮细胞和基底细胞的增殖和数量。

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Clara cell 10-kDa protein (CC10) is an inhibitor of phospholipase A2 and binds to phosphatidylinositol. It may therefore interfere with intracellular signal transduction. Bronchial CC10-reactive cells have been described by several authors. In contrast to the bronchiolar CC10-containing Clara cell, which is a progenitor cell of terminally differentiated airway epithelium, the role of bronchial CC10-reactive cells remains to be elucidated. We assessed the number of bronchial CC10-reactive cells in relation to cytokeratin (CK) expression and proliferative activity in normal, hyperplastic and squamous metaplastic epithelium. Sixty-five human bronchial mucosal specimens were investigated immunohistochemically for CK expression (CK7, CK13 and CK5/6), proliferative activity (MIB-1) and number of CC10-reactive epithelia. The proliferation fraction of CC10-reactive cells was assessed with double staining for MIB-1 and CC10. The proliferation index of the epithelium differed significantly between normal, hyperplastic and metaplastic epithelium. The number of CC10-reactive cells was inversely related to the epithelial proliferation. Bronchial CC10-reactive cells showed no proliferative activity as assessed using immunohistochemical double staining for CC10 and MIB-1. In contrast to normal and hyperplastic epithelium, squamous metaplasia disclosed CK5/6 in all epithelial layers, a loss of CK7 and a gain of CK13. We conclude that CC10-reactive cells have no progenitor role in the bronchial mucosa. However, because the proliferative activity is inversely related to the number of CC10-reactive cells, the CC10 protein may play a role in the regulation of epithelial repair. Squamous metaplasia most likely originates from basal cells.
机译:克拉拉细胞10-kDa蛋白(CC10)是磷脂酶A2的抑制剂,并与磷脂酰肌醇结合。因此,它可能会干扰细胞内信号转导。几位作者已经描述了支气管CC10反应性细胞。含支气管CC10的Clara细胞是终末分化的气道上皮的祖细胞,与此相反,支气管CC10反应性细胞的作用尚待阐明。我们评估了正常,增生和鳞状化生上皮细胞中与细胞角蛋白(CK)表达和增殖活性相关的支气管CC10反应性细胞数量。免疫组化研究了65个人支气管粘膜标本的CK表达(CK7,CK13和CK5 / 6),增殖活性(MIB-1)和CC10反应性上皮细胞的数量。用MIB-1和CC10的双重染色评估CC10反应性细胞的增殖分数。正常,增生和化生上皮之间的上皮增殖指数有显着差异。 CC10反应性细胞的数量与上皮增殖成反比。使用CC10和MIB-1的免疫组织化学双重染色评估,支气管CC10反应性细胞未显示增殖活性。与正常和增生上皮相反,鳞状化生显示所有上皮层中的CK5 / 6,CK7缺失和CK13增高。我们得出的结论是,CC10反应性细胞在支气管粘膜中没有祖细胞的作用。但是,由于增殖活性与CC10反应性细胞的数量成反比,因此CC10蛋白可能在上皮修复的调节中起作用。鳞状化生很可能起源于基底细胞。

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