Vascular endothelial growth factor increases fenestral permeability in hepatic sinusoidal endothelial cells

Yokomori, Hiroaki; Oda, Masaya; Yoshimura, Kazunori; Nagai, Toshihiro; Ogi, Mariko; Nomura, Masahiko; Ishii, Hiromasa

doi:10.1111/j.1478-3231.2003.00880.x

Cited by 85 publications

(64 citation statements)

References 25 publications

(32 reference statements)

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“…In vitro, VEGF has been shown to mediate the formation of fenestrations by choroid plexus 11 and liver endothelial cells. 13 A recent report 48 describes the loss of fenestrations in pancreatic islet endothelial cells after Cre-mediated deletion of VEGF-A, but in this experiment VEGF-A was deleted during development and its role in the adult was not addressed. Fenestrations have also been shown to be diminished in pancreatic tumors after VEGF neutralization.…”

Section: Discussionmentioning

confidence: 99%

“…Previous work in our laboratory has identified type II pneumocytes as the site of VEGF expression in the alveolus 25 ( Figure 4D, arrow). The liver, which is vascularized by a sinusoidal vascular bed 13,30 ( Figure 4F, arrowheads), uniformly expressed VEGF in hepatocytes ( Figure 4F, arrows). The hepatocytes abut the sinusoidal vasculature and are responsible for extracting nutrients and toxins from the blood as it makes its way from peripheral arteries to the central collecting vein (Figure 4F).…”

Section: Vegf Expression In the Lung Liver And Kidneymentioning

confidence: 99%

“…10 Furthermore, VEGF has been shown to induce fenestrations in endothelial cells in vitro. [11][12][13] Fenestrated blood vessels are found in many secretory organs, including kidney, choroid plexus, and the choroid layer of the eye. Recent evidence has demonstrated a loss of tumor vessel fenestrations in pancreatic tumors after VEGF receptor blockade.…”

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confidence: 99%

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Vascular Endothelial Growth Factor Localization in the Adult

Maharaj

Saint‐Geniez

Maldonado

et al. 2006

The American Journal of Pathology

254

217

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Although vascular endothelial growth factor (VEGF) has been well studied in both developmental and pathological angiogenesis, its role in mature blood vessels is poorly understood. A growing body of observations, including the side effects of anti-VEGF therapies as well as the role of soluble VEGFR1 in preeclampsia, points to an important role for VEGF in maintenance of stable blood vessels. To better understand the potential function of VEGF in mature vessels, a survey of VEGF localization in adult mice was conducted. In adult VEGF-lacZ mice, VEGF was expressed in a cell-specific manner by cells overlying fenestrated and sinusoidal blood vessels, including podocytes, choroid plexus epithelium, and hepatocytes, as well as in tissues with high metabolic demands or with secretory functions, such as cardiac and skeletal myocytes, Leydig cells, prostatic epithelium, and salivary serous epithelium. VEGF was not detected in most endothelium but was specifically expressed by aortic endothelial cells where VEGFR2 was found to be phosphorylated, indicating an autocrine loop. Additionally, VEGFR2 was constitutively phosphorylated in the liver, lung, adipose, and kidney in vivo, providing evidence consistent with a role for VEGF in adult tissues. These observations support the concept that VEGF acts in the adult to stabilize mature vessels.

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Section: Discussionmentioning

confidence: 99%

Section: Vegf Expression In the Lung Liver And Kidneymentioning

confidence: 99%

See 1 more Smart Citation

Vascular Endothelial Growth Factor Localization in the Adult

Maharaj

Saint‐Geniez

Maldonado

et al. 2006

The American Journal of Pathology

254

217

View full text Add to dashboard Cite

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].…”

Section: Angiogenesis In Liver Regenerationmentioning

confidence: 99%

Angiogenesis: multiple masks in hepatocellular carcinoma and liver regeneration

Chen

Shi

et al. 2010

Hepatol Int

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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.

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“…BSP has also been shown to promote osteoclastic resorption of mineralized surfaces (16). VEGF is able to induce the growth of new blood vessels and, in addition, it plays an important role in the maintenance and development of endothelial fenestrations (17)(18)(19)(20).…”

mentioning

confidence: 99%

Vascular Endothelial Growth Factor and E-Nitric Oxide Synthase-Mediated Regenerative Response Occurring upon Autologous and Heterologous Bone Grafts

Tetè

Zara

Vinci

et al. 2009

Int J Immunopathol Pharmacol

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Bone regeneration procedures allow oral rehabilitation with dental implants also in edentulous ridges with severe bone atrophy. The integration of grafted materials with the host tissue can initiate regenerative, inflammatory and apoptotic response. Since molecular mechanisms exist at the basis of such response, the aim of this work is to investigate, by immunohistochemical analyses, the expression of proteins involved in the graft integration process, in parallel to clinical and histological modifications, occurring on sites treated with extraoral autologous bone graft deriving from the parietal region of the calvaria (eAB), intraoral autologous bone graft deriving from mandibular ramus (iAB) and heterologous bone graft from swine (hB) in human patients. In our study, the immunohistochemical expression of BSP, VEGF, eNOS in eAB samples was significantly higher (p< 0.05) compared to values recorded in iAB and hB samples. The inflammatory response, investigated by iNOS expression, was found lower in all autologous samples (eAB and iAB) compared to hB, at statistically significant values. Moreover, the expression of the pro-apoptotic molecule, Bax, resulted significantly lower (p< 0.05) in eAB than in iAB and hB samples. These values, together with the low number of apoptotic cells detected in autologous samples, suggest a good regenerative response when extraoral autologous bone graft is used in comparison to the response from the other grafts, and also suggest the use of calvaria graft as a predictable therapeutic procedure for repairing severe bone defects in oral and maxillofacial surgery, not only by clinical and biomechanical criteria, but also from a biomolecular aspect.After dental extractions, alveolar bone undergoes remodeling phenomena, leading to both vertical and horizontal bone loss (l). In addition to these phenomena, and to the generally poor quality of the bone in the upper distal regions, maxillary sinus pneumatization process occurs, determining an insufficient residual bone height to ensure primary stability of the implant placement (2). Novel classification of residual bone in the posterior maxilla considers, besides the width and the height of the residual alveolus, also the intermaxillary relationship (3). To correct these severe bone defects and to have a good prosthetic result, the use of onlay bone grafts, in addition to sinus floor lift, represents

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Vascular endothelial growth factor increases fenestral permeability in hepatic sinusoidal endothelial cells

Cited by 85 publications

References 25 publications

Vascular Endothelial Growth Factor Localization in the Adult

Vascular Endothelial Growth Factor Localization in the Adult

Angiogenesis: multiple masks in hepatocellular carcinoma and liver regeneration

Vascular Endothelial Growth Factor and E-Nitric Oxide Synthase-Mediated Regenerative Response Occurring upon Autologous and Heterologous Bone Grafts

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