Localization of transforming growth factor-beta-expressing cells and comparison with major extracellular components in aural cholesteatoma
Localization of transforming growth factor-beta-expressing cells and comparison with major extracellular components in aural cholesteatoma
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DOI：
10.1177/000348949710600810
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发表时间：
1997-08-01
影响因子：
1.4
通讯作者：
Nerlich, A
中科院分区：
文献类型：
--
作者：
Lang, S;Schilling, V;Nerlich, A
转化生长因子- β (tgf - β)在调节细胞外基质（ECM）沉积中发挥重要作用，刺激个体基质蛋白如腱素和纤维连接蛋白的合成。胆脂瘤在ECM中表现出显著的变化，支持了细胞-基质相互作用受到干扰的观点。我们本研究的目的是通过组织化学和免疫组织化学的方法来评估tgf - β的分布，并将其与作为胆脂瘤ECM主要成分的腱素、纤维连接蛋白和胶原的沉积进行比较。我们在7例胆脂瘤间质中发现淋巴细胞和纤维组织细胞中存在tgf - β。在相应的切片中，可以看到腱素和纤维连接蛋白的显著表达，沿表皮-间质交界处呈连续带状，延伸到更深的间质。此外，在tgf - β表达的病例中，在相邻的更深的间质层中可以看到开始形成胶原纤维，表明开始发生间质纤维化。这些结果表明tgf - β可能参与刺激腱素、纤维连接蛋白和胶原蛋白的合成。此外，腱蛋白和纤维连接蛋白的表达增强为胆脂瘤中与胆脂瘤形成的增殖过程增强相关的细胞-基质相互作用失调提供了证据。
Transforming growth factor-beta (TGF-beta) plays an important role in the regulation of extracellular matrix (ECM) deposition by stimulating the synthesis of individual matrix proteins like tenascin and fibronectin. Cholesteatoma shows significant changes in the ECM, supporting the view of a disturbed cell-matrix interaction. The purpose of our present study was to evaluate the distribution of TGF-beta in comparison to the deposition of tenascin, fibronectin, and collagen as major components of the ECM in cholesteatoma (n = 12) by means of histochemistry and immunohistochemistry. We found TGF-beta in lymphocytes and fibrohistiocytes in the stroma of 7 cholesteatomas. In corresponding sections, a marked expression of tenascin and fibronectin was seen manifesting as a continuous band along the epidermal-stromal junction, extending to the deeper stroma. In addition, in those cases of TGF-beta expression, beginning collagen fibril formation was seen in adjacent deeper stroma layers, indicating beginning stromal fibrosis. These results suggest that TGF-beta may be involved in the stimulation of the synthesis of tenascin, fibronectin, and collagen. Furthermore, the enhanced expression of tenascin and fibronectin provides evidence for a deregulated cell-matrix interaction in cholesteatoma associated with the enhanced proliferative process of cholesteatoma formation.