Smad3 knock-out mice as a useful model to study intestinal fibrogenesis  被引量:3

Smad3 knock-out mice as a useful model to study intestinal fibrogenesis

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作  者:Giuliana Zanninelli Antonella Vetuschi Roberta Sferra Angela D'Angelo Amato Fratticci Maria Adelaide Continenza Maria Chiaramonte Eugenio Gaudio Renzo Caprilli Giovanni Latella 

机构地区:[1]Cattedra di Gastroenterologia,Università degli Studi di L'Aquila,L'Aquila,Italy [2]Cattedra di Anatomia Umana,Università degli Studi di L'Aquila,L'Aquila,Italy [3]Dipartimento di Medicina Sperimentale,Università degli Studi di L'Aquila,L'Aquila,Italy [4]Università degli Studi di Roma"La Sapienza" [5]Roma,Italy [6]Cattedra di Gastroenterologia I,Università degli Studi di Roma"La Sapienza",Roma,Italy

出  处:《World Journal of Gastroenterology》2006年第8期1211-1218,共8页世界胃肠病学杂志(英文版)

摘  要:AIM: To evaluate the possible differences in morphology and immunohistochemical expression of CD3, transforming growth factor 131(TGF-131), Smad7, α-smooth muscle actin (α-Sma), and collagen types Ⅰ-Ⅶ of small and large intestine in Smad3 null and wild-type mice. METHODS: Ten null and ten wild-type adult mice were sacrificed at 4 mo of age and the organs (esophagus, small and large bowel, ureters) were collected for histology(hematoxylin and eosin, Masson thrichrome, silver staining), morphometry and immunohistochemistry analysis. TGF-β1 levels of intestinal tissue homogenates were assessed by ELISA. RESULTS: No macroscopic intestinal lesions were detected both in null and wild-type mice. Histological and morphometric evaluation revealed a significant reduction in muscle layer thickness of small and large intestine in null mice as compared to wild-type mice. Immunohistochemistry evaluation showed a significant increase of CD3+T cell, TGF-β1 and Smad7 staining in the small and large intestine mucosa of Smad3 null mice as compared to wild-type mice. α-Sma and collagen Ⅰ-Ⅶ staining of small and large intestine did not differ between the two groups of mice. TGF-β1 levels of colonic tissue homogenates were significantly higher in null mice than in wildtype mice. In preliminary experiments a significant reduction of TNBS-induced intestinal fibrosis was observed in null mice as compared to wild-type mice.瞄准:为了在形态学和免疫评估可能的差别, CD3,转变生长因素 beta1 (TGF-beta1 ) , Smad7, alpha 光滑的肌肉肌动朊(alpha-Sma ) ,和骨胶原的组织化学的表示打 I-VII 小并且在 Smad3 空、野类型的老鼠的大肠。方法:十 0 和十只野类型的成年老鼠在年龄和机关的 4 瞬间被牺牲(食管,小、大的肠,输尿管) 为组织学被收集(苏木精和曙红,马森 thrichrome,染色的银) ,形态测定法和免疫组织化学分析。肠的织物 homogenates 的 TGF-beta1 层次被 ELISA 估计。结果:没有宏观的肠的损害在空、野类型的老鼠两个都被检测。组织学并且 morphometric 评估在肌肉层厚度揭示了重要减小小并且在空老鼠的大肠同样与野类型的老鼠相比。Immunohistochemistry 评估显示出染色在的 CD3+ T 房间, TGF-beta1 和 Smad7 的重要增加小并且 Smad3 空老鼠的大肠粘膜同样与野类型的老鼠相比。染色的 Alpha-Sma 和骨胶原 I-VII 小并且大肠没在二组老鼠之间不同。结肠的织物 homogenates 的 TGF-beta1 层次比在野类型的老鼠在空老鼠是显著地更高的。在初步的实验,导致 TNBS 的肠的纤维变性的重要减小作为与野类型的老鼠相比在空老鼠被观察。结论:Smad3 空老鼠是一个有用模型调查在肠的发炎和纤维变性表明小径的 TGF-beta/Smad 的在活体内角色。

关 键 词:Transforming growth factor TGF-13 FIBROSIS Smad proteins 

分 类 号:R-332[医药卫生] R574

 

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