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- Title
Angiotensin-II and vascular endothelial growth factor interaction plays an important role in rat liver fibrosis development
- Authors
Yoshiji, Hitoshi; Kuriyama, Shigeki; Noguchi, Ryuichi; Ikenaka, Yasuhide; Kitade, Mitsuteru; Kaji, Kosuke; Yoshii, Junichi; Yanase, Koji; Yamazaki, Masaharu; Asada, Kiyoshi; Tsujimoto, Tatsuhiro; Akahane, Takemi; Uemura, Masahito; Fukui, Hiroshi
- Abstract
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.
- Subjects
VASCULAR endothelial growth factors; ANGIOTENSIN II; ANGIOTENSINS; LIVER diseases; FIBROSIS; LIVER cells
- Publication
Hepatology Research, 2006, Vol 36, Issue 2, p124
- ISSN
1386-6346
- Publication type
Article
- DOI
10.1016/j.hepres.2006.07.003