Angiopoietin/Tie Receptors System may Play a Role During Reconstruction and Capillarization of the Hepatic Sinusoids after Partial Hepatectomy and Liver Necrosis in Rats.

肝窦内皮细胞和肝细胞在肝部分切除和坏死后数量增加，并通过与星状细胞的相互作用促进窦的重建和毛细血管化。这种相互作用的机制是通过血管生成素和血管形成所必需的受体来评估的。血管生成素-1、血管生成素-2和Tie-2 mRNA的表达在大鼠70%肝切除并重建肝窦后168小时，以及四氯化碳（CC14）给予大鼠肝窦毛细血管形成48小时均有所增加。在正常大鼠的窦状内皮细胞和星状细胞以及cc14中毒大鼠的活化星状细胞中检测Tie-2 mRNA的表达。血管生成素-1和血管生成素-2 mRNA在正常大鼠Kupffer细胞、窦状内皮细胞和星状细胞中均可检测到，但在cc14中毒后活化的星状细胞和巨噬细胞中表达增加。血管生成素和Tie-2在70%肝切除大鼠和cc14中毒大鼠的坏死区域沿鼻窦进行免疫组织化学染色。血管生成素-1和血管生成素-2可能通过Tie-2受体与星状细胞和血管内皮细胞相互作用，参与了部分切除坏死后大鼠肝窦的重建和毛细血管化。

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 underling 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 168 hours after 70% liver resection with sinusoidal reconstruction in rats, and also at 48 hours with sinusoidal capillarization in the liver of rats given carbon tetrachloride(CC14). Tie-2 mRNA expression was detected in sinusoidal endothelial cells and stellate cells isolated from normal rats, and in activated stellate cells from CC14-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 CC14-intoxication. Both angiopoietins and Tie-2 were immunohistochemically stained along the sinusoids of 70% hepatectomized rats and in necrotic areas of CC14-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.