Expressions of Vascular Endothelial Growth Factor in Nonparenchymal as Well as Parenchymal Cells in Rat Liver after Necrosis

Ishikawa, Kinya; Mochida, Satoshi; Mashiba, Shoji; Inao, Mie; Matsui, Ayako; Ikeda, Hitoshi; Ohno, Akihiko; Shibuya, Masabumi; Fujiwara, Kenji

doi:10.1006/bbrc.1998.9984

Cited by 78 publications

(60 citation statements)

References 24 publications

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“…Hepatic VEGF (also known as VEGFA) increases in response to many forms of liver injury and after partial hepatectomy (35, 37,38,[40][41][42][43]. Knockdown of hepatic VEGF with antisense oligonucleotides can exacerbate toxic injury to the liver (35), whereas infusion of VEGF can ameliorate toxic injury (44)(45)(46) and increases hepatocyte proliferation (38) and liver weight after partial hepatectomy (3,4).…”

Section: Regulation Of Recruitment Of Bone Marrow Spcsmentioning

confidence: 99%

Liver sinusoidal endothelial cells and liver regeneration

2013

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Liver sinusoidal endothelial cells (LSECs) have long been noted to contribute to liver regeneration after liver injury. In normal liver, the major cellular source of HGF is the hepatic stellate cell, but after liver injury, HGF expression has been thought to increase markedly in proliferating LSECs. However, emerging data suggest that even after injury, LSEC expression of HGF does not increase greatly. In contrast, bone marrow progenitor cells of LSECs (BM SPCs), which are rich in HGF, are recruited to the liver after injury. This Review examines liver regeneration from the perspective that BM SPCs that have been recruited to the liver, rather than mature LSECs, drive liver regeneration.

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Section: Regulation Of Recruitment Of Bone Marrow Spcsmentioning

confidence: 99%

Liver sinusoidal endothelial cells and liver regeneration

2013

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“…It has been demonstrated that expression of VEGF is up-regulated during liver fibrosis, and its expression is increased in activated hepatic stellate cells (HSCs) (Medina et al, 2004;Tugues et al, 2007;Rosmorduc et al, 1999;Maria De Souza et al, 2006). Activated HSCs can express VEGF and VEGF receptors in the liver after CCl 4 intoxication (Ishikawa et al, 1999;Ankoma-Sey et al, 2000). Inflammatory mediators cause the HSCs to differentiate into myofibroblasts.…”

Section: Figmentioning

confidence: 99%

Neutralization of ADAM8 ameliorates liver injury and accelerates liver repair in carbon tetrachloride-induced acute liver injury

Zhu

Wan

et al. 2014

J. Toxicol. Sci.

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-Although some studies have described the function of ADAM8 (a disintegrin and metalloprotease 8) related with rheumatoid arthritis, cancer and asthma, etc., the concrete role of ADAM8 in acute liver injury is still unknown. So mice respectively received anti-ADAM8 monoclonal antibody (mAb) of 100 μg/100 μl, 200 μg/100 μl or 300 μg/100 μl in PBS or PBS pre-injection. Then acute liver injury was induced in the mice by intraperitoneal (i.p.) injection of carbon tetrachloride (CCl 4 ). Serum AST and ALT level, Haematoxylin-eosin (H&E) staining, the expression level of vascular endothelial growth factor (VEGF), cytochrome P450 1A2 (CYP1A2) and proliferating cell nuclear antigen (PCNA) were detected in the mice after CCl 4 administration. Our results showed that anti-ADAM8 mAb pre-injection could effectively lower AST and ALT levels (P < 0.05 or P < 0.01) and reduce liver injury (P < 0.05 or P < 0.01), induce the expression of VEGF, CYP1A2 and PCNA (P < 0.05 or P < 0.01) in dose-dependent manner compared with the control mice which received PBS pre-injection. In summary, our study suggested that ADAM8 might promote liver injury by inhibiting the proliferation of hepatocytes, angiogenesis and affecting the metabolism function of liver during acute liver injury induced by CCl 4 . Anti-ADAM8 mAb injection might be suitable as a potential method for acute liver injury therapy.

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“…7 During the fibrotic progression of chronic liver diseases (CLDs), activated and myofibroblast-like HSCs (HSC/MFs) play a major profibrogenic role together with portal (myo)fibroblast and, possibly, bone marrow-derived stem cells, giving rise to hepatic populations of highly proliferative, profibrogenic, and contractile myofibroblast-like cells (MFs). 10 -16 Possible interplay and/or association between fibrogenesis and angiogenesis in CLDs is now suggested and supported by several findings: 1) angiogenesis and upregulation of vascular endothelial growth factor (VEGF) expression has been documented in different models of acute and chronic liver injury 7,[17][18][19][20][21] as well as in specimens from human fibrotic/cirrhotic liver and hepatocellular carcinoma 7,[22][23][24] ; 2) in HSCs, hypoxia has been shown to up-regulate expression of VEGF, 20,[25][26][27] VEGF receptor type I (fms-like tyrosine kinase receptor or Flt-1), 20,25 and collagen type I 20 ; 3) VEGF has been proposed to directly stimulate proliferation and expression of ␣1(I)-procollagen mRNA in activated rat HSCs 21 ; and 4) paracrine expression of VEGF by rat HSCs as well as by hepatocytes has been shown to regulate the phenotype (ie, fenestration and CD-31 expression) of liver sinusoidal endothelial cells, 28 a feature of possible relevance in CLDs. Data concerning expression of angiopoietins are, at present, much more limited.…”

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confidence: 93%