Placenta growth factor. Potentiation of vascular endothelial growth factor bioactivity, in vitro and in vivo, and high affinity binding to Flt-1 but not to Flk-1/KDR.

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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Transgenic Overexpression of Vascular Endothelial Growth Factor-B Isoforms by Endothelial Cells Potentiates Postnatal Vessel Growth In Vivo and In Vitro

Circulation Research ◽

10.1161/01.res.0000182631.33638.77 ◽

2005 ◽

Vol 97 (6) ◽

Cited By ~ 38

Author(s):

Arne W. Mould ◽

Sonia A. Greco ◽

Marian M. Cahill ◽

Ian D. Tonks ◽

Daniela Bellomo ◽

...

Keyword(s):

Vascular Endothelial Growth Factor ◽

Endothelial Cells ◽

Growth Factor ◽

Vascular Endothelial ◽

Factor B ◽

Vessel Growth ◽

Endothelial Growth Factor

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Regulation of Vascular Endothelial Growth Factor by Tamoxifen in vitro and in vivo

Gynecologic and Obstetric Investigation ◽

10.1159/000070190 ◽

2003 ◽

Vol 55 (2) ◽

pp. 119-124 ◽

Cited By ~ 3

Author(s):

Michael D. Mueller ◽

Elizabeth A. Pritts ◽

Charles J. Zaloudek ◽

Ekkehard Dreher ◽

Robert N. Taylor

Keyword(s):

Vascular Endothelial Growth Factor ◽

Growth Factor ◽

Vascular Endothelial ◽

Endothelial Growth Factor

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Total saponins from Albizia julibrissin inhibit vascular endothelial growth factor-mediated angiogenesis in vitro and in vivo

Molecular Medicine Reports ◽

10.3892/mmr.2015.3228 ◽

2015 ◽

Vol 11 (5) ◽

pp. 3405-3413 ◽

Cited By ~ 9

Author(s):

WEIWEI CAI ◽

YUE LI ◽

QINGQING YI ◽

FENGSHAN XIE ◽

BIN DU ◽

...

Keyword(s):

Vascular Endothelial Growth Factor ◽

Growth Factor ◽

Vascular Endothelial ◽

Albizia Julibrissin ◽

Endothelial Growth Factor

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Vascular Endothelial Growth Factor Inhibits the Development of Dendritic Cells and Dramatically Affects the Differentiation of Multiple Hematopoietic Lineages In Vivo

Blood ◽

10.1182/blood.v92.11.4150 ◽

1998 ◽

Vol 92 (11) ◽

pp. 4150-4166 ◽

Cited By ~ 624

Author(s):

Dmitry Gabrilovich ◽

Tadao Ishida ◽

Tsunehiro Oyama ◽

Sophia Ran ◽

Vladimir Kravtsov ◽

...

Keyword(s):

Stem Cells ◽

Vascular Endothelial Growth Factor ◽

Dendritic Cells ◽

Growth Factor ◽

System Control ◽

Vascular Endothelial ◽

Almost All ◽

Endothelial Growth Factor

Abstract Defective function of dendritic cells (DC) in cancer has been recently described and may represent one of the mechanisms of tumor evasion from immune system control. We have previously shown in vitro that vascular endothelial growth factor (VEGF), produced by almost all tumors, is one of the tumor-derived factors responsible for the defective function of these cells. In this study, we investigated whether in vivo infusion of recombinant VEGF could reproduce the observed DC dysfunction. Continuous VEGF infusion, at rates as low as 50 ng/h (resulting in serum VEGF concentrations of 120 to 160 pg/mL), resulted in a dramatic inhibition of dendritic cell development, associated with an increase in the production of B cells and immature Gr-1+ myeloid cells. Infusion of VEGF was associated with inhibition of the activity of the transcription factor NF-κB in bone marrow progenitor cells. Experiments in vitro showed that VEGF itself, and not factors released by VEGF-activated endothelial cells, affected polypotent stem cells resulting in the observed abnormal hematopoiesis. These data suggest that VEGF, at pathologically relevant concentrations in vivo, may exert effects on pluripotent stem cells that result in blocked DC development as well as affect many other hematopoietic lineages.

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