Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
3311504 | Hepatology Research | 2006 | 6 Pages |
Abstract
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.
Keywords
Related Topics
Health Sciences
Medicine and Dentistry
Gastroenterology
Authors
Hitoshi Yoshiji, Shigeki Kuriyama, Ryuichi Noguchi, Yasuhide Ikenaka, Mitsuteru Kitade, Kosuke Kaji, Junichi Yoshii, Koji Yanase, Masaharu Yamazaki, Kiyoshi Asada, Tatsuhiro Tsujimoto, Takemi Akahane, Masahito Uemura, Hiroshi Fukui,