Sinusoidal endothelial cell proliferation and expression of angiopoietin/Tie family in regenerating rat liver

Sato, Takashi; El-Assal, Osama N.; Ono, Takashi; Yamanoi, Akira; Dhar, Dipok Kumar; Nagasue, Naofumi

doi:10.1016/s0168-8278(00)00109-4

Cited by 113 publications

(102 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…44,45 Hepatic expression of Ang-1 and Ang-2 is increased following PH in rats, but at a later phase than VEGF. 37 Both factors exert opposing actions: in the presence of VEGF, Ang-2 seems to augment angiogenesis early during regeneration, while in the absence of VEGF, Ang-2 inhibits vascular growth at later stages. 37 The profile of activation of PDGF and its receptors during liver regeneration (Table 1) suggests a potential role in maturation of the newly formed sinusoids.…”

Section: Liver Regeneration: a Model For Hepatic Angiogenesismentioning

confidence: 99%

“…37 Both factors exert opposing actions: in the presence of VEGF, Ang-2 seems to augment angiogenesis early during regeneration, while in the absence of VEGF, Ang-2 inhibits vascular growth at later stages. 37 The profile of activation of PDGF and its receptors during liver regeneration (Table 1) suggests a potential role in maturation of the newly formed sinusoids. 35 FGF receptors FGF-R1 (Flg) and FGF-R2 (Bek) are increased in hepatocytes during liver regeneration following PH, 46 but there is limited evidence of their contribution to vascular growth.…”

Section: Liver Regeneration: a Model For Hepatic Angiogenesismentioning

confidence: 99%

See 1 more Smart Citation

Angiogenesis in chronic inflammatory liver disease

et al. 2004

View full text Add to dashboard Cite

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.

show abstract

Section: Liver Regeneration: a Model For Hepatic Angiogenesismentioning

confidence: 99%

Section: Liver Regeneration: a Model For Hepatic Angiogenesismentioning

confidence: 99%

Angiogenesis in chronic inflammatory liver disease

et al. 2004

View full text Add to dashboard Cite

show abstract

“…2 During liver regeneration in adults, for example in the rat or mouse partial hepatectomy (PHx) model, hepatocytes proliferate to form avascular parenchymal islands, and stimulate and attract LSECs, [3][4][5] through vascular endothelial growth factor (VEGF) and other angiogenic signals. [6][7][8] On the other hand, LSECs can play an angiogenesis-independent protective role on hepatocytes through vascular endothelial growth factor receptor 1 (VEGFR1) signaling. LeCouter et al 9 showed that PHxinduced VEGF up-regulation can induce LSEC proliferation by binding to VEGFR2, and can induce LSECs to secrete interleukin-6 (IL-6) and hepatocyte growth factor (HGF) to promote hepatocyte proliferation through VEGFR1.…”

mentioning

confidence: 99%

Disruption of the transcription factor recombination signal‐binding protein‐Jκ (RBP‐J) leads to veno‐occlusive disease and interfered liver regeneration in mice†

Wang

Hou

et al. 2009

Hepatology

View full text Add to dashboard Cite

Liver sinusoid (LS) endothelial cells (LSECs) support hepatocytes in resting liversand proliferate during liver regeneration to revascularize regenerated liver parenchyma. We report that recombination signal-binding protein-J (RBP-J), the critical transcription factor mediating Notch signaling, regulates both resting and regenerating LSECs. Conditional deletion of RBP-J resulted in LSEC proliferation and a veno-occlusive disease-like phenotype in the liver, as manifested by liver congestion, deposition of fibrin-like materials in LSs, edema in the space of Disse, and increased apoptosis of hepatocytes. Regeneration of liver was remarkably impaired, with reduced LSEC proliferation and destroyed sinusoidal structure. LSEC degeneration was obvious in the regenerating liver of RBP-J-deficient mice, with some LSECs losing cytoplasm, and organelles protruding into the remnant plasma-membrane of LSs to hamper the microcirculation and intensify veno-occlusive disease during liver regeneration. Hepatocytes were also degenerative, as shown by dilated endoplasmic reticulum, decreased proliferation, and increased apoptosis during liver regeneration. Molecular analyses revealed that the dynamic expression of several related molecules-such as vascular endothelial growth factor, vascular endothelial growth factor receptors 1 and 2, interleukin-6, and hepatocyte growth factor-was disturbed. Conclusion: Notch/RBP-J signaling may play dual roles in LSECs: in resting liver it represses proliferation, and in regenerating liver it supports proliferation and functional differentiation. (

show abstract

“…As a potent survival factor of endothelial cells, VEGF promotes the proliferation of endothelial cells and regulates vascular permeability of LSECs [30,31]. VEGF production is accompanied by increased expression of VEGFR-1 on hepatocytes and HSCs and of VEGFR-1 and VEGFR-2 on LSECs [25,27,32,33]. After binding to the VEGFR-1 of hepatocytes, VEGF can induce autocrine proliferation of hepatocytes [29].…”

Section: Angiogenesis In Liver Regenerationmentioning

confidence: 99%

“…However, in the absence of VEGF, Ang-2 leads to vessels regression [47,48]. In the regenerating liver, VEGF expression peaked at 72 h. Angiopoietin/Tie factors peaked at 96 h except for Ang-2, which gradually increased and peaked at 168 h. It is possible that in the presence of VEGF, Ang-2 augments angiogenesis in the early phase of regeneration and inhibits angiogenesis in the absence of VEGF when the regeneration is completed [25,32,49,50].…”

Section: Angiogenesis In Liver Regenerationmentioning

confidence: 99%

Angiogenesis: multiple masks in hepatocellular carcinoma and liver regeneration

Chen

Shi

et al. 2010

Hepatol Int

View full text Add to dashboard Cite

Hepatocellular carcinoma (HCC) is naturally resistant to radiotherapy and cytotoxic chemotherapy, leaving surgery as the mainstream therapeutic approach. However, the 5-year recurrence rate after curative resection is as high as 61.5%. The background hepatitis B-or C-induced cirrhosis and the presence of micrometastases at the time of surgery have been regarded as two main causes of recurrence. Recently, accumulating evidence suggests that growth factors and cytokines released during the physiological process of post-surgical liver regeneration could induce the activation of dormant micrometastatic lesions. The establishment of neovasculature to support either liver regeneration or HCC growth involves multiple cell types including liver sinusoidal endothelial cells, Kupffer cells, hepatic stellate cells, and circulating endothelial progenitors. The crosstalks among these cells are driven by multiple molecules and signaling pathways, including vascular endothelial growth factors and their receptors, platelet-derived growth factor, the angiopoietin/Tie family, hepatocyte growth factor/c-Met signaling, and others. Anti-angiogenic agent targeting liver cancer vasculature has been reported to be able to generate limited survival benefit of the patients. In this review, discussions are focused on various angiogenic mechanisms of HCC and liver regeneration, as well as the prevailing anti-angiogenic strategies.

show abstract

Sinusoidal endothelial cell proliferation and expression of angiopoietin/Tie family in regenerating rat liver

Cited by 113 publications

References 23 publications

Angiogenesis in chronic inflammatory liver disease

Angiogenesis in chronic inflammatory liver disease

Disruption of the transcription factor recombination signal‐binding protein‐Jκ (RBP‐J) leads to veno‐occlusive disease and interfered liver regeneration in mice†

Angiogenesis: multiple masks in hepatocellular carcinoma and liver regeneration

Contact Info

Product

Resources

About