Riedl S E, Faissner A, Schlag P, Von Herbay A, Koretz K, Möller P
Department of Surgery, Heidelberg University, Germany.
Gastroenterology. 1992 Aug;103(2):400-6. doi: 10.1016/0016-5085(92)90827-l.
Tenascin is a fibroblast product and extracellular matrix protein probably excerting a fibronectin-antagonizing role. Tenascin is broadly distributed interstitially during embryogenesis but restricted to a small range of structures in normal adult tissues. Using tenascin antibodies and an indirect immunoperoxidase method, normal colon, colitis, colon adenomas, and colorectal carcinomas were examined for tissue distribution of tenascin. Normal mucosa displayed a sparce meshwork of microfibrillar tenascin in the lamina propria. The basement membrane was tenascin negative at the bottom of the crypt and developed into a positive band steadily broadening towards the mucosal surface. In colitis, this polarity was effaced; the basement membrane was a broad tenascin-positive band nearly throughout while interstitial tenascin was moderately increased. Loss of polarity in tenascin content of the basement membrane was a constant feature of adenomas, inconsistently paralleled by structural alterations in surface qualities and continuity of tenascin pattern of the basement membrane. These were most pronounced in carcinomas, where this interface was often discontinuous and had a rough surface; in addition, interstitial tenascin was considerably increased. In carcinomas, the rough surface aspect of the tenascin pattern of the basement membrane was correlated with presence of lymph node metastases (P = 0.04). It is concluded that alterations in tenascin pattern and content reflect complex disturbances in the interaction of inflamed/neoplastic colon epithelium and underlying matrix, leading to an organoid induction of tenascin in the inflammatory context and to induction together with structural abnormalities in neoplasia.
腱生蛋白是一种成纤维细胞产物和细胞外基质蛋白,可能发挥纤连蛋白拮抗作用。腱生蛋白在胚胎发育过程中间质广泛分布,但在正常成年组织中局限于小范围结构。使用腱生蛋白抗体和间接免疫过氧化物酶方法,对正常结肠、结肠炎、结肠腺瘤和结肠直肠癌进行腱生蛋白组织分布检查。正常黏膜在固有层显示微纤维状腱生蛋白的稀疏网络。隐窝底部的基底膜腱生蛋白呈阴性,向黏膜表面逐渐形成一条不断变宽的阳性带。在结肠炎中,这种极性消失;基底膜几乎全程是一条宽的腱生蛋白阳性带,而间质腱生蛋白适度增加。基底膜腱生蛋白含量极性的丧失是腺瘤的一个恒定特征,基底膜腱生蛋白模式的表面质量和连续性的结构改变与之不完全平行。这些在癌中最为明显,其中该界面常不连续且表面粗糙;此外,间质腱生蛋白显著增加。在癌中,基底膜腱生蛋白模式的粗糙表面与淋巴结转移的存在相关(P = 0.04)。结论是,腱生蛋白模式和含量的改变反映了炎症/肿瘤性结肠上皮与下层基质相互作用中的复杂紊乱,导致在炎症背景下类器官诱导腱生蛋白,并在肿瘤形成过程中与结构异常一起诱导。