Expression of Vascular Endothelial Growth Factor C Correlates with Lymphatic Vessel Density and Prognosis in Human Gastroesophageal Junction Carcinoma

Onkologie ◽  
2012 ◽  
Vol 35 (3) ◽  
pp. 88-93 ◽  
Author(s):  
Li Ping Yang ◽  
Lin Chen Fu ◽  
Hong Guo ◽  
Liang Xi Xie
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Lymphatic Vessel ◽  
Gastroesophageal Junction ◽  
Vessel Density ◽  
Vascular Endothelial ◽  
Lymphatic Vessel Density ◽  
Gastroesophageal Junction Carcinoma ◽  
Factor C ◽  
Endothelial Growth Factor

scholarly journals Distinct vascular endothelial growth factor signals for lymphatic vessel enlargement and sprouting

2007 ◽  
Vol 204 (6) ◽  
pp. 1431-1440 ◽  
Author(s):  
Maria Wirzenius ◽  
Tuomas Tammela ◽  
Marko Uutela ◽  
Yulong He ◽  
Teresa Odorisio ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Lymphatic Vessel ◽  
Lymphatic Vessels ◽  
Mouse Skin ◽  
Vegf Receptor ◽  
Vascular Endothelial ◽  
Factor C ◽  
Endothelial Growth Factor

Lymphatic vessel growth, or lymphangiogenesis, is regulated by vascular endothelial growth factor-C (VEGF-C) and -D via VEGF receptor 3 (VEGFR-3). Recent studies suggest that VEGF, which does not bind to VEGFR-3, can also induce lymphangiogenesis through unknown mechanisms. To dissect the receptor pathway that triggers VEGFR-3–independent lymphangiogenesis, we used both transgenic and adenoviral overexpression of placenta growth factor (PlGF) and VEGF-E, which are specific activators of VEGFR-1 and -2, respectively. Unlike PlGF, VEGF-E induced circumferential lymphatic vessel hyperplasia, but essentially no new vessel sprouting, when transduced into mouse skin via adenoviral vectors. This effect was not inhibited by blocking VEGF-C and -D. Postnatal lymphatic hyperplasia, without increased density of lymphatic vessels, was also detected in transgenic mice expressing VEGF-E in the skin, but not in mice expressing PlGF. Surprisingly, VEGF-E induced lymphatic hyperplasia postnatally, and it did not rescue the loss of lymphatic vessels in transgenic embryos where VEGF-C and VEGF-D were blocked. Our data suggests that VEGFR-2 signals promote lymphatic vessel enlargement, but unlike in the blood vessels, are not involved in vessel sprouting to generate new lymphatic vessels in vivo.

scholarly journals Topical VEGF-C/D Inhibition Prevents Lymphatic Vessel Ingrowth into Cornea but Does Not Improve Corneal Graft Survival

2020 ◽  
Vol 9 (5) ◽  
pp. 1270
Author(s):  
Ann-Charlott Salabarria ◽  
Manuel Koch ◽  
Alfrun Schönberg ◽  
Elisabeth Zinser ◽  
Deniz Hos ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
High Risk ◽  
Immune Cells ◽  
Lymphatic Vessel ◽  
Corneal Transplantation ◽  
Lymphatic Vessels ◽  
Vascular Endothelial ◽  
Factor C ◽  
Endothelial Growth Factor

Vascular endothelial growth factor-C/D (VEGF-C/D) regulates lymphangiogenesis. Ingrowth of lymphatic vessels is negatively associated with corneal transplantation success. In this study, we therefore analyzed the effect local blockade of VEGF-C/D has on inflamed corneas. We used the murine model of suture-induced neovascularization and subsequent high-risk corneal transplantation. Mice were treated with a VEGF-C/D trap prior to transplantation. Topical inhibition of VEGF-C/D significantly reduced lymphatic vessel ingrowth, but increased Macrophage numbers in the cornea. Furthermore, corneal transplantation success was not improved by the topical application of the compound. This study demonstrates that local VEGF-C/D inhibition is insufficient to increases corneal transplantation success, likely due to interaction with immune cells.

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