scholarly journals A hydrophobic gelatin fiber sheet promotes secretion of endogenous vascular endothelial growth factor and stimulates angiogenesis

RSC Advances ◽  
2020 ◽  
Vol 10 (42) ◽  
pp. 24800-24807
Author(s):  
Yosuke Mizuno ◽  
Tetsushi Taguchi
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Electrospun Fiber ◽  
Vascular Endothelial ◽  
Fiber Sheet ◽  
Endothelial Growth Factor

In vivo long-term growth factor-free angiogenesis by LPS-mimicking C16-modified gelatin based electrospun fiber sheet.

Vascular endothelial growth factor activity after switching of bisphosphonate treatment for metastatic breast cancer

2009 ◽  
Vol 62 (5) ◽  
pp. 474-476 ◽  
Author(s):  
E Amir ◽  
M Trinkaus ◽  
C E Simmons ◽  
G Dranitsaris ◽  
M J Clemons
Keyword(s):  
Breast Cancer ◽  
Vascular Endothelial Growth Factor ◽  
Zoledronic Acid ◽  
Growth Factor ◽  
Metastatic Breast ◽  
Vascular Endothelial ◽  
Pretreated Patients ◽  
Endothelial Growth Factor

Background:Recent data have shown a fall in vascular endothelial growth factor (VEGF) concentrations after bisphosphonate (BP) treatment in BP-naïve patients. It has therefore been proposed that BPs may have in vivo anti-VEGF effects.Aims:To explore whether VEGF concentrations change after administration of a more potent BP in patients receiving long-term BP treatment.Methods:31 patients with breast cancer who had progressive metastatic bone disease despite treatment with early-generation BPs were switched to zoledronic acid. Serum VEGF concentrations were measured at baseline, and weeks 1, 2, 3, 4, 8 and 12.Results:VEGF concentration per platelet count did not change significantly at any time during the 12 weeks after treatment with zoledronic acid.Conclusions:Switching to zoledronic acid did not suppress circulating serum VEGF concentrations in BP-pretreated patients. Novel approaches to assess the effect of BPs on the bone milieu may provide further insight into the possible antiangiogenic properties of BPs.

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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