scholarly journals Cycloamylose‐nanogel drug delivery system‐mediated intratumor silencing of the vascular endothelial growth factor regulates neovascularization in tumor microenvironment

2014 ◽  
Vol 105 (12) ◽  
pp. 1616-1625 ◽  
Author(s):  
Hidetaka Fujii ◽  
Masaharu Shin‐Ya ◽  
Shigeo Takeda ◽  
Yoshihide Hashimoto ◽  
Sada‐atsu Mukai ◽  
...  
Keyword(s):  
Drug Delivery ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Tumor Microenvironment ◽  
Drug Delivery System ◽  
Delivery System ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

scholarly journals Induction of Vascular Endothelial Growth Factor by Hypoxia Is Modulated by a Phosphatidylinositol 3-Kinase/Akt Signaling Pathway in Ha-ras-Transformed Cells Through a Hypoxia Inducible Factor-1 Transcriptional Element

Blood ◽  
1997 ◽  
Vol 90 (9) ◽  
pp. 3322-3331 ◽  
Author(s):  
Nathalie M. Mazure ◽  
Eunice Y. Chen ◽  
Keith R. Laderoute ◽  
Amato J. Giaccia
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Tumor Microenvironment ◽  
Kinase Activity ◽  
Hypoxia Inducible Factor ◽  
Transformed Cells ◽  
Vascular Endothelial ◽  
Phosphatidylinositol 3 Kinase ◽  
Hypoxia Inducible Factor 1 ◽  
Endothelial Growth Factor

Abstract Tumor angiogenesis, the development of new blood vessels, is a highly regulated process that is controlled genetically by alterations in oncogene and tumor suppressor gene expression and physiologically by the tumor microenvironment. Previous studies indicate that the angiogenic switch in Ras-transformed cells may be physiologically promoted by the tumor microenvironment through the induction of the angiogenic mitogen, vascular endothelial growth factor (VEGF). In this report, we show Ras-transformed cells do not use the downstream effectors c-Raf-1 or mitogen activated protein kinases (MAPK) in signaling VEGF induction by hypoxia as overexpression of kinase-defective alleles of these genes does not inhibit VEGF induction under low oxygen conditions. In contrast to the c-Raf-1/MAP kinase pathway, hypoxia increases phosphatidylinositol 3-kinase (PI 3-kinase) activity in a Ras-dependent manner, and inhibition of PI 3-kinase activity genetically and pharmacologically results in inhibition of VEGF induction. We propose that hypoxia modulates VEGF induction in Ras-transformed cells through the activation of a stress inducible PI 3-kinase/Akt pathway and the hypoxia inducible factor-1 (HIF-1) transcriptional response element.

Biodegradable Polyglycolide Endovascular Coils Promote Wall Thickening and Drug Delivery in a Rat Aneurysm Model

Neurosurgery ◽  
2001 ◽  
Vol 49 (5) ◽  
pp. 1187-1195 ◽  
Author(s):  
John M. Abrahams ◽  
Mark S. Forman ◽  
M. Sean Grady ◽  
Scott L. Diamond
Keyword(s):  
Drug Delivery ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Cellular Proliferation ◽  
Wall Thickening ◽  
Type I ◽  
Vascular Endothelial ◽  
Adult Rats ◽  
Luminal Diameter ◽  
Endothelial Growth Factor

ABSTRACT OBJECTIVE We designed biodegradable polyglycolide coils (BPCs) and compared the histopathological response to the coils with that to platinum Guglielmi detachable coils (GDCs), after insertion into ligated common carotid arteries (CCAs) of adult rats. BPCs were also tested for use in local drug delivery. METHODS Segments (4-mm) of unmodified BPCs, unmodified GDCs, or BPCs coated with Type I bovine collagen and recombinant human vascular endothelial growth factor-165 (500 μg/ml) were inserted into ligated CCAs of adult rats for 14 days, and specimens were compared with contralateral CCA control specimens. RESULTS Arterial segments with BPCs exhibited substantially increased wall thickening, compared with GDCs (0.33 mm versus 0.10 mm, P < 0.005), which reduced the luminal diameter by 40%, relative to untreated contralateral control specimens (P < 0.05, n = 6). Arterial segments with BPCs also exhibited a marked reduction (P < 0.05, n = 6) in luminal area (0.72 ± 0.93 mm2), with marked cellular proliferation within the coil diameter, indicating coil integration. Arterial segments with collagen/recombinant human vascular endothelial growth factor-coated BPCs also exhibited a marked 2.9-fold increase (P < 0.005, n = 5) in wall thickness (0.29 ± 0.11 mm) and a 34% reduction in luminal diameter, compared with contralateral control vessels. There was marked proliferation of cells within the coil lumen of vessels treated with BPCs with collagen/recombinant human vascular endothelial growth factor. CONCLUSION In this feasibility study, BPCs enhanced the vascular response of CCA segments, compared with GDCs, and were also suitable for local protein delivery to the vessel lumen, under conditions of stasis and arterial pressurization of vascular cells.

Transport of vascular endothelial growth factor dictates on-chip angiogenesis in tumor microenvironment

2021 ◽  
Vol 33 (3) ◽  
pp. 031910
Author(s):  
Jyotsana Priyadarshani ◽  
Prasoon Awasthi ◽  
Pratyaksh Karan ◽  
Soumen Das ◽  
Suman Chakraborty
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Tumor Microenvironment ◽  
Vascular Endothelial ◽  
On Chip ◽  
Endothelial Growth Factor
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