Angiotensin-II and vascular endothelial growth factor interaction plays an important role in rat liver fibrosis development

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• 作者：Hitoshi Yoshiji ; Shigeki Kuriyama ; Ryuichi Noguchi ; Yasuhide Ikenaka ; Mitsuteru Kitade ; Kosuke Kaji ; Junichi Yoshii ; Koji Yanase ; Masaharu Yamazaki ; Kiyoshi Asada et al.
• 关键词：Angiogenesis ; Angiotensin-II ; Hepatic stellate cell ; Liver fibrosis ; VEGF
• 刊名：Hepatology Research
• 出版年：2006
• 出版时间：October 2006
• 年：2006
• 卷：36
• 期：2
• 页码：124-129
• 全文大小：894 K

文摘

Both angiotensin-II (AT-II) and vascular endothelial growth factor (VEGF) have been shown to play important roles in the progression of liver fibrosis. However, the interaction of AT-II with VEGF in the liver fibrosis has not been elucidated yet. The aim of the current study was to elucidate a possible association between these molecules, especially in conjunction with the hepatic stellate cells (HSC). The effect of AT-II type 1 receptor blocker (ARB) was assessed on several indices of choline-deficient l-amino acid-defined (CDAA)-induced liver fibrogenesis. This ARB significantly suppressed liver fibrosis development along with suppression of the VEGF expression and neovascularization in the liver. In the cultured activated HSC, AT-II induced VEGF in a dose- and time-dependent manner. ARB and LY333531, a protein kinase C (PKC) inhibitor, attenuated this augmentation. These results indicated that AT-II and VEGF interaction played an important role in liver fibrosis development, and that in the activated HSC, AT-II utilized type 1 receptor and PKC as an intracellular signaling pathway to induce VEGF.