scholarly journals Potential Role of A2BAdenosine Receptors on Proliferation/Migration of Fetal Endothelium Derived from Preeclamptic Pregnancies

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Jesenia Acurio ◽  
Felipe Troncoso ◽  
Patricio Bertoglia ◽  
Carlos Salomon ◽  
Claudio Aguayo ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Proliferation ◽  
Signaling Pathway ◽  
Adenosine Receptor ◽  
Protein Level ◽  
Normal Pregnancy ◽  
Endothelial Cell Proliferation ◽  
Vegf Signaling ◽  
Vegf Signaling Pathway ◽  
In Cells

To investigate the functionality ofA2Badenosine receptor (A2BAR) and the nitric oxide (NO) and vascular endothelial growth factor (VEGF) signaling pathway in the endothelial cell proliferation/migration during preeclampsia, we used human umbilical vein endothelial cells (HUVECs) isolated from normal pregnanciesn=15or pregnancies with preeclampsian=15. Experiments were performed in presence or absence of the nonselective adenosine receptor agonist NECA, theA2BAR selective antagonist MRS-1754, and the nitric oxide synthase (NOS) inhibitor L-NAME. Results indicated that cells from preeclampsia exhibited a significant higher protein level ofA2BAR and logEC50for NECA-mediated proliferation than normotensive pregnancies. The stimulatory effect of NECA (10 μM, 24 h) on cell proliferation was prevented by MRS-1754 (5 nM) coincubation only in cells from normotensive pregnancies. Nevertheless, L-NAME (100 μM, 24 h) reduced the NECA-induced cell proliferation/migration in HUVEC from normal pregnancy; however in preeclampsia only NECA-induced cell proliferation was reduced by L-NAME. Moreover, NECA increased protein nitration and abundance of VEGF in cells from normal pregnancy and effect prevented by MRS-1754 coincubation. Nevertheless, in preeclampsia NECA did not affect the protein level of VEGF. In conclusion HUVECs from preeclampsia exhibit elevated protein level ofA2BAR and impairment ofA2BAR-mediated NO/VEGF signaling pathway.

scholarly journals Impaired A2A adenosine receptor/nitric oxide/VEGF signaling pathway in fetal endothelium during late- and early-onset preeclampsia

2012 ◽  
Vol 9 (2) ◽  
pp. 215-226 ◽  
Author(s):  
Carlos Escudero ◽  
Patricio Bertoglia ◽  
Myriam Hernadez ◽  
Cristian Celis ◽  
Marcelo Gonzalez ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Signaling Pathway ◽  
Adenosine Receptor ◽  
Early Onset ◽  
A2a Adenosine Receptor ◽  
Vegf Signaling ◽  
Early Onset Preeclampsia ◽  
Vegf Signaling Pathway

Abstract 117: RhoC Regulates VEGF-induced Signaling in Endothelial Cells

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Luke Hoeppner ◽  
Sutapa Sinha ◽  
Ying Wang ◽  
Resham Bhattacharya ◽  
Shamit Dutta ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Vascular Permeability ◽  
Rho Gtpase ◽  
Endothelial Cell Migration ◽  
Calcium Flux ◽  
Endothelial Cell Proliferation ◽  
Vegf Receptor ◽  
Vegf Signaling

Vascular permeability factor/vascular endothelial growth factor A (VEGF) is a central regulator of angiogenesis and potently promotes vascular permeability. VEGF plays a key role in the pathologies of heart disease, stroke, and cancer. Therefore, understanding the molecular regulation of VEGF signaling is an important pursuit. Rho GTPase proteins play various roles in vasculogenesis and angiogenesis. While the functions of RhoA and RhoB in these processes have been well defined, little is known about the role of RhoC in VEGF-mediated signaling in endothelial cells and vascular development. Here, we describe how RhoC modulates VEGF signaling to regulate endothelial cell proliferation, migration and permeability. We found VEGF stimulation activates RhoC in human umbilical vein endothelial cells (HUVECs), which was completely blocked after VEGF receptor 2 (VEGFR-2) knockdown indicating that VEGF activates RhoC through VEGFR-2 signaling. Interestingly, RhoC knockdown delayed the degradation of VEGFR-2 compared to control siRNA treated HUVECs, thus implicating RhoC in VEGFR-2 trafficking. In light of our results suggesting VEGF activates RhoC through VEGFR-2, we sought to determine whether RhoC regulates vascular permeability through the VEGFR-2/phospholipase Cγ (PLCγ) /Ca 2+ /eNOS cascade. We found RhoC knockdown in VEGF-stimulated HUVECs significantly increased PLC-γ1 phosphorylation at tyrosine 783, promoted basal and VEGF-stimulated eNOS phophorylation at serine 1177, and increased calcium flux compared with control siRNA transfected HUVECs. Taken together, our findings suggest RhoC negatively regulates VEGF-induced vascular permeability. We confirmed this finding through a VEGF-inducible zebrafish model of vascular permeability by observing significantly greater vascular permeability in RhoC morpholino (MO)-injected zebrafish than control MO-injected zebrafish. Furthermore, we showed that RhoC promotes endothelial cell proliferation and negatively regulates endothelial cell migration. Our data suggests a scenario in which RhoC promotes proliferation by upregulating -catenin in a Wnt signaling-independent manner, which in turn, promotes Cyclin D1 expression and subsequently drives cell cycle progression.

PTEN regulate angiogenesis through PI3K/Akt/VEGF signaling pathway in human pancreatic cancer cells

2009 ◽  
Vol 331 (1-2) ◽  
pp. 161-171 ◽  
Author(s):  
Jiachi Ma ◽  
Hirozumi Sawai ◽  
Nobuo Ochi ◽  
Yoichi Matsuo ◽  
Donghui Xu ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Human Pancreatic Cancer ◽  
Vegf Signaling ◽  
Pancreatic Cancer Cells ◽  
Vegf Signaling Pathway

Dihydroartemisinin inhibits endothelial cell proliferation through the suppression of the ERK signaling pathway

2015 ◽  
Vol 35 (5) ◽  
pp. 1381-1387 ◽  
Author(s):  
FENGYUN DONG ◽  
HU TIAN ◽  
SUHUA YAN ◽  
LIQUN LI ◽  
XIAOFENG DONG ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cell ◽  
Signaling Pathway ◽  
Erk Signaling ◽  
Endothelial Cell Proliferation

Emodin alleviated pulmonary inflammation in rats with LPS-induced acute lung injury through inhibiting the mTOR/HIF-1α/VEGF signaling pathway

2020 ◽  
Vol 69 (4) ◽  
pp. 365-373 ◽  
Author(s):  
Xiaoqian Li ◽  
Cong Shan ◽  
Zhonghua Wu ◽  
Hongji Yu ◽  
Aidong Yang ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Signaling Pathway ◽  
Pulmonary Inflammation ◽  
Vegf Signaling ◽  
Vegf Signaling Pathway
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