Molecular mechanisms for changes in hepatic protein synthesis induced by schistosomiasis infection in mice.
Molecular mechanisms for changes in hepatic protein synthesis induced by schistosomiasis infection in mice.
复制标题
血吸虫病感染小鼠肝脏蛋白质合成变化的分子机制。
DOI：
10.1021/bi00295a005
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发表时间：
1983
期刊：
影响因子：
2.9
通讯作者：
Shafritz,DA
中科院分区：
文献类型：
--
作者：
Zern,MA;Saber,MA;Shafritz,DA
Mark A.Zern，*Mohamed A.Saber，5和David A.Shafritz摘要：对感染曼氏血吸虫的小鼠和对照小鼠进行了为期12周的连续评估。感染的小鼠体重增加的速度与对照组相同，但从第六周开始，它们的肝脏变大，肉芽肿和纤维组织，并出现低蛋白血症。为了评价白蛋白和I型胶原基因表达的调节，从感染和对照小鼠中提取总RNA，并翻译到依赖于mRNA的兔网织红细胞裂解物系统中。与对照相比，感染肝脏的RNA可使蛋白质合成减少1.5-3倍。无细胞产物十二烷基硫酸钠-聚丙烯酰胺凝胶电泳法显示，感染小鼠白蛋白减少，I型前胶原合成增加。无细胞产物的免疫沉淀血吸虫病是一种主要的热带寄生虫病。尽管2亿血吸虫感染者中的大多数人没有表现出疾病，但相当数量的人有相当大的发病率和慢性肝病的死亡率(Warren，1980)。曼氏血吸虫病虫卵滞留在肝窦内会引起炎症反应，导致肉芽肿形成，最终导致肝纤维化。这种纤维化的特点是沉积在厚带中，而肝实质通常保存完好(Dunn&Kamel，1981)。然而，在某些情况下，长期肝纤维化后会发生低蛋白血症(Cook等人，1974)。
Mark A. Zern,* Mohamed A. Saber, 5 and David A. Shafritz abstract: Mice infected with Schistosoma mansoni and littermate controls were evaluated serially for 12 weeks. In-fected mice gained weight at the same rate as controls, but starting with the sixth week their liversbecame enlarged with granulomas and fibrous tissue, and they developed hypoalbuminemia. To evaluate the regulation of the albumin and type I collagen gene expression, total RNA was isolated from infected and control mice and translated in an mRNA-de-pendent rabbit reticulocyte lysate system. Protein synthesis was decreased 1.5-3-fold with RNA from infected vs. control liver. Sodium dodecyl sulfate-polyacrylamide gel electro-phoresis of the cell-free products showed a reduction in al-bumin but an increase in type I procollagen synthesis in in-fected mice. Immunoprecipitation of the cell-free productSchistosomiasis is a major parasitic disease involving tropical regions. Although most of the 200 million people with schistosome infection show no disease, appreciable numbers have substantial morbidity and mortality from chronic liver disease (Warren, 1980). The eggs of Schistosomiasis mansoni cause an inflammatory response when trapped in liver sinu-soids, leading to granuloma formation and ultimately to hepatic fibrosis. This fibrosis is characteristically deposited in thick bands, whereas the hepatic parenchyma is typically well-preserved (Dunn & Kamel, 1981). In some cases, however, hypoalbuminemia occurs after long-term hepatic fibrosis (Cook et al., 1974).