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表达牛细胞视黄酸结合蛋白的转基因小鼠的发病机制:(转基因/视黄酸/CRABP/发病机制)

Pathogenesis in Transgenic Mice Expressing Bovine Cellular Retinoic Acid-Binding Protein: (transgenic/retinoic acid/CRABP/pathogenesis).

作者信息

Wei Li-Na, Lee Chih-Hao, Chang Shu-Ling, Chu Ya-Shu

机构信息

Department of Microbiology and Immunology, Chang Gung Medical College, Tao-Yuan, Taiwan, R.O.C.

出版信息

Dev Growth Differ. 1992 Aug;34(4):479-488. doi: 10.1111/j.1440-169X.1992.00479.x.

DOI:10.1111/j.1440-169X.1992.00479.x
PMID:37281365
Abstract

Transgenic mice with ectopic expression of bovine CRABP under the control of the human metallotheionein IIA promoter have shown a variety of pathological consequences. Expression of the transgene has been detected in most of the tissues examined, including heart, lung, liver, spleen, kidney, intestine, testis, and ovary, except pancreas. Two independent lines have been able to produce normal non-transgenic F animals of both sexes but only female transgenic progenies. All of these F female transgenic animals derived from both lines are sterile, and the ovaries from these animals appear to be significantly smaller as compared to their non-transgenic littermates. Histopathological examinations have shown no maturing follicles in these transgenic ovaries in which abnormal cells have been observed. Another independent line has generated transgenic F animals which have been growing retardly. These animals all have small spleen and liver and have become very sick at the age of 4 to 5 weeks. Histopathological examinations on these transgenic progenies have shown hepatocytes to be reduced in the cytoplasmic portion in which glycogen is highly depleted. The spleen is poorly developed as no well organized germinal centers can be observed in the spleen sections of these transgenic animals.

摘要

在人金属硫蛋白IIA启动子控制下异位表达牛CRABP的转基因小鼠已表现出多种病理后果。在所检测的大多数组织中均检测到转基因的表达,包括心脏、肺、肝脏、脾脏、肾脏、肠道、睾丸和卵巢,但胰腺除外。两个独立品系均能够产生正常的非转基因雌雄F代动物,但仅能产生雌性转基因后代。来自这两个品系的所有这些F代雌性转基因动物均不育,并且与它们的非转基因同窝仔相比,这些动物的卵巢明显更小。组织病理学检查显示,在这些观察到异常细胞的转基因卵巢中没有成熟卵泡。另一个独立品系产生了生长迟缓的转基因F代动物。这些动物均脾脏和肝脏较小,并且在4至5周龄时已病得很重。对这些转基因后代的组织病理学检查显示,肝细胞的细胞质部分减少,其中糖原高度消耗。脾脏发育不良,因为在这些转基因动物的脾脏切片中未观察到组织良好的生发中心。

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Pathogenesis in Transgenic Mice Expressing Bovine Cellular Retinoic Acid-Binding Protein: (transgenic/retinoic acid/CRABP/pathogenesis).表达牛细胞视黄酸结合蛋白的转基因小鼠的发病机制:(转基因/视黄酸/CRABP/发病机制)
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Biol Reprod. 1997 Jan;56(1):125-32. doi: 10.1095/biolreprod56.1.125.

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