scholarly journals In Vivo Detection of Human Vascular Endothelial Growth Factor Promoter Activity in Transgenic Mouse Skin

2000 ◽  
Vol 157 (1) ◽  
pp. 103-110 ◽  
Author(s):  
Jiro Kishimoto ◽  
Ritsuko Ehama ◽  
Yimin Ge ◽  
Takashi Kobayashi ◽  
Toshio Nishiyama ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Transgenic Mouse ◽  
Promoter Activity ◽  
Mouse Skin ◽  
Vascular Endothelial ◽  
In Vivo Detection ◽  
Endothelial Growth Factor

scholarly journals Bioluminescence Imaging of Vascular Endothelial Growth Factor Promoter Activity in Murine Mammary Tumorigenesis

2007 ◽  
Vol 6 (5) ◽  
pp. 7290.2007.00029 ◽  
Author(s):  
Shannon L. Faley ◽  
Keiko Takahashi ◽  
Cornelia E. Crooke ◽  
Joshua T. Beckham ◽  
Takuya Tomemori ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Mammary Tumor ◽  
Promoter Activity ◽  
Fluorescent Protein ◽  
T Antigen ◽  
The Body ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

Vascular endothelial growth factor (VEGF) is a major inducer of angiogenesis. We generated a transgenic reporter mouse, VEGF-GL, in which an enhanced green fluorescent protein-luciferase fusion protein is expressed under the control of a human VEGF-A promoter. The VEGF-GL mouse exhibited intense bioluminescence throughout the body at 1 week of age. The signals rapidly declined to a relatively low level as the mice grew. The adult VEGF-GL mouse showed restricted bioluminescence to the areas undergoing wound healing. In contrast, the VEGF-GL mice, which were crossed with mouse mammary tumor virus-polyoma virus middle T antigen transgenic mammary tumor mice, exhibited prominent bioluminescence in the tumors, correlating with VEGF transcription. Tumor bioluminescence was observed in the bigenic mice as early as 8 weeks, before tumors were palpable, and the signals increased with tumor growth. In conclusion, the VEGF-GL mouse permits longitudinal and quantitative assessment of VEGF promoter activity in vivo. The model should facilitate understanding of the molecular controls and pathways that regulate VEGF transcription in vivo.

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 Role of vascular endothelial growth factor in inducing production of angiopoetin-1 – in vivo study in Fisher rats

2017 ◽  
Vol 68 (4) ◽  
pp. 326-329
Author(s):  
Piotr Barć ◽  
Tomasz Płonek ◽  
Dagmara Baczyńska ◽  
Artur Pupka ◽  
Wojciech Witkiewicz ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
In Vivo Study ◽  
Vascular Endothelial ◽  
Angiopoetin 1 ◽  
Endothelial Growth Factor

Mice overexpressing placenta growth factor exhibit increased vascularization and vessel permeability

2002 ◽  
Vol 115 (12) ◽  
pp. 2559-2567 ◽  
Author(s):  
Teresa Odorisio ◽  
Cataldo Schietroma ◽  
M. Letizia Zaccaria ◽  
Francesca Cianfarani ◽  
Cecilia Tiveron ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Adult Life ◽  
Growth Factor Receptor ◽  
Vascular Endothelial ◽  
Placenta Growth Factor ◽  
Vessel Permeability ◽  
Exact Function ◽  
Endothelial Growth Factor

Placenta growth factor (PlGF) is a member of the vascular endothelial growth factor (VEGF) family, comprising at least five cytokines specifically involved in the regulation of vascular and/or lymphatic endothelium differentiation. Several lines of evidence indicate a role for PlGF in monocyte chemotaxis and in potentiating the activity of VEGF, but the exact function of this cytokine is not fully understood. To define the biological role of PlGF in vivo, we have produced a transgenic mouse model overexpressing this factor in the skin by using a keratin 14 promoter cassette. Our data indicate that PlGF has strong angiogenic properties in both fetal and adult life. PlGF overexpression results in a substantial increase in the number,branching and size of dermal blood vessels as well as in enhanced vascular permeability. Indeed, intradermally injected recombinant PlGF was able to induce vessel permeability in wild-type mice. The analysis of vascular endothelial growth factor receptor 1/flt-1 and vascular endothelial growth factor receptor 2/flk-1 indicates that the two receptors are induced in the skin endothelium of transgenic mice suggesting that both are involved in mediating the effect of overexpressed PlGF.

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