首页> 外文期刊>Hepatology research: the official journal of the Japan Society of Hepatology >Angiopoietin/tie receptors system may play a role during reconstruction and capillarization of the hepatic sinusoids after partial hepatectomy and liver necrosis in rats.
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Angiopoietin/tie receptors system may play a role during reconstruction and capillarization of the hepatic sinusoids after partial hepatectomy and liver necrosis in rats.

机译:血管生成素/领带受体系统可能在大鼠部分肝切除和肝坏死后肝窦的重建和毛细血管化过程中发挥作用。

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摘要

Sinusoidal endothelial cells and hepatocytes increase in number after partial resection and necrosis of the liver, and contribute to both reconstruction and capillarization of the sinusoids through interaction with stellate cells. The mechanism underlying such interaction was evaluated regarding angiopoietins and tie receptors essential for blood vessel formation. Hepatic mRNA expressions of angiopoietin-1, angiopoietin-2 and tie-2 were increased at 168h after 70% liver resection with sinusoidal reconstruction in rats, and also at 48h with sinusoidal capillarization in the liver of rats given carbon tetrachloride (CCl(4)). Tie-2 mRNA expression was detected in sinusoidal endothelial cells and stellate cells isolated from normal rats, and in activated stellate cells from CCl(4)-intoxicated rats. The mRNA expressions of angiopoietin-1 and angiopoietin-2 were detectable in Kupffer cells, sinusoidal endothelial cells and stellate cells in normal rats, but increased in activated stellate cells and macrophages after CCl(4)-intoxication. Both angiopoietins and tie-2 were immunohistochemically stained along the sinusoids of 70% hepatectomized rats and in necrotic areas of CCl(4)-intoxicated rats. Angiopoietin-1 and angiopoietin-2 may be involved in both reconstruction and capillarization of the sinusoids in rat liver after partial resection and necrosis through interaction between stellate cells and sinusoidal and vascular endothelial cells via tie-2 receptor.
机译:肝部分切除和坏死后,窦状内皮细胞和肝细胞数量增加,并通过与星状细胞相互作用而促进窦状窦的重建和毛细血管化。关于血管生成素和血管形成必不可少的tie受体,评估了这种相互作用的基础机制。肝切除70%并进行正弦重建的大鼠在168h时血管生成素1,血管生成素2和tie-2的肝mRNA表达增加,并且在四氯化碳(CCl(4) )。在从正常大鼠分离的正弦血管内皮细胞和星状细胞中,以及在CCl(4)中毒的大鼠的活化星状细胞中检测到Tie-2 mRNA表达。在正常大鼠的Kupffer细胞,窦状内皮细胞和星状细胞中可检测到血管生成素1和血管生成素2的mRNA表达,但在CCl(4)中毒后,活化的星状细胞和巨噬细胞中的表达升高。沿70%肝切除大鼠的正弦曲线和CCl(4)中毒大鼠的坏死区域对血管生成素和tie-2进行了免疫组织化学染色。血管生成素-1和血管生成素-2可能通过st-2受体通过星状细胞与窦状和血管内皮细胞之间的相互作用,参与部分切除和坏死后大鼠肝中窦的重建和毛细血管化。

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