Vascular Endothelial Growth Factor Receptor Blockade by SU5416 Combined With Pulsatile Shear Stress Causes Apoptosis and Subsequent Proliferation of Apoptosis-Resistant Endothelial Cells

CHEST Journal ◽  
2005 ◽  
Vol 128 (6) ◽  
pp. 610S-611S ◽  
Author(s):  
Seiichiro Sakao ◽  
Laimute Taraseviciene-Stewart ◽  
Jong Deog Lee ◽  
Kathy Wood ◽  
Carlyne D. Cool ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Endothelial Cells ◽  
Shear Stress ◽  
Growth Factor ◽  
Growth Factor Receptor ◽  
Receptor Blockade ◽  
Vascular Endothelial ◽  
Pulsatile Shear Stress ◽  
Endothelial Growth Factor

scholarly journals Transient Exposure of Endothelial Cells to Doxorubicin Leads to Long-Lasting Vascular Endothelial Growth Factor Receptor 2 Downregulation

Cells ◽  
2022 ◽  
Vol 11 (2) ◽  
pp. 210
Author(s):  
Silvia Graziani ◽  
Luca Scorrano ◽  
Giovanna Pontarin
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Endothelial Cells ◽  
Protein Synthesis ◽  
Growth Factor ◽  
Drug Withdrawal ◽  
Growth Factor Receptor ◽  
Vascular Endothelial ◽  
P53 Expression ◽  
Endothelial Growth Factor

Doxorubicin (Dox) is an effective antineoplastic drug with serious cardiotoxic side effects that persist after drug withdrawal and can lead to heart failure. Dysregulation of vascular endothelium has been linked to the development of Dox-induced cardiotoxicity, but it is unclear whether and how transient exposure to Dox leads to long-term downregulation of Endothelial Vascular Endothelial Growth Factor Receptor type2 (VEGFR2), essential for endothelial cells function. Using an in vitro model devised to study the long-lasting effects of brief endothelial cells exposure to Dox, we show that Dox leads to sustained protein synthesis inhibition and VEGFR2 downregulation. Transient Dox treatment led to the development of long-term senescence associated with a reduction in VEGFR2 levels that persisted days after drug withdrawal. By analyzing VEGFR2 turnover, we ruled out that its downregulation was depended on Dox-induced autophagy. Conversely, Dox induced p53 expression, reduced mTOR-dependent translation, and inhibited global protein synthesis. Our data contribute to a mechanistic basis to the permanent damage caused to endothelial cells by short-term Dox treatment.

scholarly journals Correction: Vascular Endothelial Growth Factor Receptor-2 Couples Cyclo-Oxygenase-2 with Pro-Angiogenic Actions of Leptin on Human Endothelial Cells

PLoS ONE ◽  
2019 ◽  
Vol 14 (9) ◽  
pp. e0223400
Author(s):  
Elena Garonna ◽  
Kathleen M. Botham ◽  
Graeme M. Birdsey ◽  
Anna M. Randi ◽  
Ruben R. Gonzalez-Perez ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Endothelial Cells ◽  
Growth Factor ◽  
Growth Factor Receptor ◽  
Vascular Endothelial ◽  
Human Endothelial Cells ◽  
Endothelial Growth Factor

Ibuprofen and indomethacin differentially regulate vascular endothelial growth factor and its receptors in ductus arteriosus endothelial cells

2017 ◽  
Vol 28 (3) ◽  
pp. 432-437 ◽  
Author(s):  
Hannes Sallmon ◽  
Sandra Akanbi ◽  
Sven C. Weber ◽  
Alexander Gratopp ◽  
Cornelia Rheinländer ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Endothelial Cells ◽  
Growth Factor ◽  
Ductus Arteriosus ◽  
Growth Factor Receptor ◽  
Vascular Endothelial ◽  
Aortic Endothelial Cells ◽  
Expression Levels ◽  
Ductal Closure ◽  
Endothelial Growth Factor

AbstractBackgroundCyclooxygenase inhibitors are widely applied to facilitate ductal closure in preterm infants. The mechanisms that lead to patent ductus arteriosus closure are incompletely understood. Vascular endothelial growth factor plays pivotal roles during ductal closure and remodelling.AimThe aim of this study was to investigate the effects of ibuprofen and indomethacin on the expression of vascular endothelial growth factor and its receptors in a primary rat ductus arteriosus endothelial cell culture.MethodsProtein expression of vascular endothelial growth factor and vascular endothelial growth factor receptor 1 and 2 was confirmed in rat ductus arteriosus and aorta by immunofluorescence staining. Fetal rat endothelial cells were isolated from ductus arteriosus and aorta using immunomagnetic cell sorting and treated with ibuprofen or indomethacin. mRNA expression levels were assessed by quantitative polymerase chain reaction analysis.ResultsIn ductal endothelial cells, ibuprofen significantly induced vascular endothelial growth factor and its receptor 2, but not receptor 1, whereas indomethacin did not alter the expression levels of the vascular endothelial growth factor system. In contrast, ibuprofen significantly induced vascular endothelial growth factor and its receptors 1 and 2 in aortic endothelial cells, whereas indomethacin only induced vascular endothelial growth factor receptor 2.ConclusionOur results indicate differential effects of ibuprofen and indomethacin on the expression levels of the vascular endothelial growth factor system in ductus arteriosus endothelial cells. In addition, vessel-specific differences between ductal and aortic endothelial cells were found. Further in vivo studies are needed to elucidate the biological significance of these findings.

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