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硒诱导的结节性再生性增生大鼠模型中肝血窦向毛细血管的转变:免疫光镜和免疫电镜研究

Transformation of sinusoids into capillaries in a rat model of selenium-induced nodular regenerative hyperplasia: an immunolight and immunoelectron microscopic study.

作者信息

Dubuisson L, Boussarie L, Bedin C A, Balabaud C, Bioulac-Sage P

机构信息

Laboratoire des Interactions Cellulaires, Université de Bordeaux II, France.

出版信息

Hepatology. 1995 Mar;21(3):805-14.

PMID:7875679
Abstract

The oral administration of selenium (Se) to young rats induces, over a 2-month period, the formation of nodular regenerative hyperplasia with sinusoidal damage around nodules. Perinodular areas located in zone 1 comprise atrophic hepatocytes and capillarized sinusoids without fibrosis. We used this unique model of capillarization without fibrosis to investigate the temporal relationship between the process of capillarization and changes occurring in the deposition of components of the extracellular matrix. After 2 weeks of intoxication, type III collagen and fibronectin were stable, but laminin and type IV collagen had increased in zone 1, resulting in the formation of septae between portal tracts. Even at 8 weeks, these two components still formed the principal deposits in perinodular zones. Electron microscopy showed already at 1 week in zone 1 that part of the endothelial wall had detached from hepatocytes. Sinusoidal endothelial cells progressively acquired certain of the characteristics of a vascular endothelium, some proliferated, and perisinusoidal cells transformed into myofibroblasts, surrounded by deposits of laminin and type IV collagen. These results indicate that both laminin and type IV collagen are involved in capillarization without fibrosis and in angiogenesis; fibronectin would not seem to play a role.

摘要

给幼鼠口服硒(Se),在2个月的时间里会诱导形成结节性再生性增生,并伴有结节周围的窦性损伤。位于1区的结节周围区域包括萎缩的肝细胞和毛细血管化的血窦,无纤维化。我们利用这种无纤维化的毛细血管化独特模型,研究毛细血管化过程与细胞外基质成分沉积变化之间的时间关系。中毒2周后,III型胶原蛋白和纤连蛋白稳定,但1区的层粘连蛋白和IV型胶原蛋白增加,导致门管之间形成间隔。即使在8周时,这两种成分仍是结节周围区域的主要沉积物。电子显微镜显示,在1周时1区的部分内皮壁已与肝细胞分离。血窦内皮细胞逐渐获得血管内皮的某些特征,一些细胞增殖,窦周细胞转化为肌成纤维细胞,周围有层粘连蛋白和IV型胶原蛋白沉积。这些结果表明,层粘连蛋白和IV型胶原蛋白都参与了无纤维化的毛细血管化和血管生成;纤连蛋白似乎不起作用。

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