Increased Expressions of Vascular Endothelial Growth Factor and Its Receptors,flt-1 andKDR/flk-1, in Regenerating Rat Liver

Mochida, Satoshi; Ishikawa, Kinya; Inao, Mie; Shibuya, Masabumi; Fujiwara, Kenji

doi:10.1006/bbrc.1996.1329

Cited by 117 publications

(102 citation statements)

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“…7 In this study we implicate hypoxia, one of the specific microenvironments in solid tumors or during wound healing in the differential expression of the VEGF receptors, Flt-1 and Flk-1, in stellate cells. Hypoxia up-regulated the expression of the mRNA for the VEGF receptor, Flt-1, in T6 monolayer cultures, however, mRNA expression of the VEGF receptor, Flk-1, was unchanged in response to hypoxia.…”

Section: Discussionmentioning

confidence: 85%

“…6 Emerging pieces of evidence suggest that VEGF may be an important angiogenic factor during hepatic injury and repair. 7,8 In response to liver injury, VEGF may enhance the regenerative potential of residual hepatocytes and that of nonparenchymal cells. 7,8 We have previously shown that the nonparenchymal hepatic cell, the hepatic stellate cell, expresses receptors for VEGF: Flt-1 and Flk-1.…”

mentioning

confidence: 99%

“…7,8 In response to liver injury, VEGF may enhance the regenerative potential of residual hepatocytes and that of nonparenchymal cells. 7,8 We have previously shown that the nonparenchymal hepatic cell, the hepatic stellate cell, expresses receptors for VEGF: Flt-1 and Flk-1. 9 This observation suggests that stellate cells are also cellular targets for VEGF during hepatic wound healing and carcinogenesis.…”

mentioning

confidence: 99%

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Hypoxic stimulation of vascular endothelial growth factor expression in activated rat hepatic stellate cells

2000

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Section: Discussionmentioning

confidence: 85%

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confidence: 99%

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confidence: 99%

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Hypoxic stimulation of vascular endothelial growth factor expression in activated rat hepatic stellate cells

2000

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“…Liver regeneration is dependent on the formation of proper vasculature via angiogenesis. 2,36,37 Additionally, MMP-9 has been implicated in angiogenesis and VEGF expression in osteoclast recruitment and carcinogenesis. 38,39 Therefore, one possible mechanism for decreased hepatic regeneration in MMP-9 Ϫ/Ϫ animals is attributable to diminished or altered vasculature formation kinetics.…”

Section: Discussionmentioning

confidence: 99%

Matrix metalloproteinase-9 is an important factor in hepatic regeneration after partial hepatectomy in mice

et al. 2006

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Partial hepatectomy triggers hepatocyte proliferation, hepatic matrix remodeling, and hepatocyte apoptosis, all of which are important processes in the regenerating liver. Previous studies have shown an increase in the levels of matrix metalloproteinases gelatinase A (MMP-2) and gelatinase B (MMP-9) after partial hepatectomy. The goal of this study was to investigate the role of MMP-9 in liver regeneration after partial hepatectomy. A 70% hepatectomy or sham laparotomy was performed in wild-type or MMP-9 -deficient (MMP-9 ؊/؊ ) mice. Hepatic regeneration was determined by liver weight/total body weight ratios and BrdU staining, which was used to a calculate mitotic index at several times postoperatively. Cytokine and growth factor expression was evaluated by Luminex™ bead-based ELISA and Western blots. Finally, the effect of MMP-9 on apoptosis was measured using TUNEL and caspase expression. The MMP-9 ؊/؊ animals had a delayed hepatic regenerative response when compared with wild-type controls. The MMP-9 -deficient animals expressed significantly less VEGF, HGF, and TNF-␣ between days 2 and 3 post-hepatectomy. Apoptosis, as measured by TUNEL staining and caspase expression, was decreased in the MMP-9 ؊/؊ . In conclusion, MMP-9 plays an important role in liver regeneration after partial hepatectomy by affecting matrix remodeling, as well as cytokine, growth factor, and caspase expression.

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“…VEGF is upregulated in periportal hepatocytes shortly after PH, 36,40 and aside from its autocrine action to induce hepatocellular growth, it stimulates surrounding ECs in a paracrine fashion. 41 Its involvement in liver regeneration-associated angiogenesis has been shown by (1) the inhibition of hepatocellular and sinusoidal EC proliferation achieved by injecting rats with a mAb anti-VEGF at the time of PH, and (2) the significant potentiation of hepatocellular and sinusoidal EC proliferation by exogenous VEGF injection simultaneously with PH.…”

Section: Liver Regeneration: a Model For Hepatic Angiogenesismentioning

confidence: 99%

Angiogenesis in chronic inflammatory liver disease

et al. 2004

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Intrahepatic hypoxia may occur during the inflammatory and fibrotic processes that characterize several chronic liver diseases of viral and autoimmune origin. As a consequence, new vascular structures are formed to provide oxygen and nutrients. Angiogenesis involves a tightly regulated network of cellular and molecular mechanisms that result in the formation of functional vessels. Of particular importance are growth factors, molecules involved in matrix remodeling and cell migration, and vessel maturation-related factors. In recent years, a number of studies have examined the expression and function of many pro-and antiangiogenic molecules in the setting of nontumoral chronic liver diseases and liver regeneration. This review examines the potential pathogenetic role of angiogenesis in the context of viral hepatitis, cirrhosis, autoimmune hepatitis, primary biliary cirrhosis, and alcoholic liver disease. The future perspectives for research in this field are outlined.

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Increased Expressions of Vascular Endothelial Growth Factor and Its Receptors,flt-1 andKDR/flk-1, in Regenerating Rat Liver

Cited by 117 publications

References 0 publications

Hypoxic stimulation of vascular endothelial growth factor expression in activated rat hepatic stellate cells

Hypoxic stimulation of vascular endothelial growth factor expression in activated rat hepatic stellate cells

Matrix metalloproteinase-9 is an important factor in hepatic regeneration after partial hepatectomy in mice

Angiogenesis in chronic inflammatory liver disease

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