scholarly journals Canagliflozin Inhibits Human Endothelial Cell Proliferation and Tube Formation

2019 ◽  
Vol 10 ◽  
Author(s):  
Ghazaleh Behnammanesh ◽  
Zane E. Durante ◽  
Kelly J. Peyton ◽  
Luis A. Martinez-Lemus ◽  
Scott M. Brown ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cell ◽  
Tube Formation ◽  
Human Endothelial Cell ◽  
Endothelial Cell Proliferation

CASIN and AMD3100 enhance endothelial cell proliferation, tube formation and sprouting

2020 ◽  
Vol 130 ◽  
pp. 104001 ◽  
Author(s):  
Batuhan Mert Kalkan ◽  
Sezer Akgol ◽  
Deniz Ak ◽  
Dogacan Yucel ◽  
Gulen Guney Esken ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cell ◽  
Tube Formation ◽  
Endothelial Cell Proliferation

Induction of endothelial proliferation and angiogenesis through activating the ERK1/2/EGF pathway mediate by CXC chemokine receptor 2 by chemokine (C-X-C motif) ligand 1.

2013 ◽  
Vol 31 (6_suppl) ◽  
pp. 138-138 ◽  
Author(s):  
Makito Miyake ◽  
Steve Goodison ◽  
Evan Gomes ◽  
Wasia Rizwani ◽  
Shanti Ross ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Chemokine Receptor ◽  
Cellular Proliferation ◽  
Human Endothelial Cell ◽  
Endothelial Cell Proliferation ◽  
Cxc Chemokine ◽  
Inhibition Of Angiogenesis

138 Background: Endothelial cell growth and proliferation are critical for tumoral angiogenesis. We report here that blockade of Chemokine (C-X-C motif) ligand 1 (CXCL1) results in reduction of human endothelial cell proliferation and its ability to induce angiogenesis. Methods: Two human endothelial cell lines, HUVEC and HDMEC, were used in the in vitro assays. Proliferation assay and matrigel tube formation assay were performed to test the inhibitory effect of anti-CXCL antibody on the activity of endothelial cells in vitro. Matrigel plug assay in nude mice was performed to test the in vivo angiogenic activity of CXCL1. Results: CXCL1 interacts with its receptor CXC chemokine Receptor 2 and induces endothelial cell proliferation, whereas blockade of CXCL1 is associated with reduction in cellular proliferation through a decrease in levels of cyclin D and cdk4 and inhibition of angiogenesis through EGF and ERK 1/2. Targeting CXCL1 inhibits neoangiogenesis but has no effect on disrupting established vasculature. Furthermore targeting CXCL1 is associated with reduction in migration of human endothelial cells in an in vitro model. Additionally, neutralizing antibody against CXCL1 in a xenograft angiogenesis model resulted in inhibition of angiogenesis. Conclusions: CXCL1-induced regulation of angiogenesis has not been studied extensively in human cancers, thus these findings illustrate a novel contribution of CXCL1 interactions in pathological angiogenesis. Therefore, the ability to selectively modulate CXCL1, specifically in tumoral angiogenesis, may promote the development of novel oncologic therapeutic strategies.

scholarly journals Roundabout4 Suppresses Glioma-Induced Endothelial Cell Proliferation, Migration and Tube Formation in Vitro by Inhibiting VEGR2-Mediated PI3K/AKT and FAK Signaling Pathways

2015 ◽  
Vol 35 (5) ◽  
pp. 1689-1705 ◽  
Author(s):  
Heng Cai ◽  
Yixue Xue ◽  
Zhen Li ◽  
Yi Hu ◽  
Zhenhua Wang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Signaling Pathways ◽  
Conditioned Medium ◽  
Tube Formation ◽  
Endothelial Cell Proliferation ◽  
Akt Inhibitor ◽  
Over Expression

Background and Aims: Endothelial cell (EC) proliferation, migration, and tube formation are the critical steps for tumor angiogenesis, which is involved in the formation of new tumor blood vessels. Roundabout4 (Robo4), a new member of Robo proteins family, is specifically expressed in endothelial cells. This study aimed to investigate the effects of Robo4 on glioma-induced endothelial cell proliferation, migration and tube formation in vitro. Methods and Results: We found that Robo4 was endogenously expressed in Human Brain Microvascular Endothelial Cells (HBMECs), while Robo4 was significantly down-regulated in endothelial cells cultured in glioma conditioned medium. Robo4 over-expression remarkably suppressed glioma-induced endothelial cell proliferation, migration and tube formation in vitro. In addition, Robo4 influenced the glioma-induced angiogenesis via binding to its ligand Slit2. Further studies demonstrated that the knockdown of Robo4 up-regulated the phosphorylation of VEGFR2, PI3K, AKT and FAK in EC cultured in glioma conditioned medium. VEGFR2 inhibitor SU-1498, AKT inhibitor LY294002 and FAK inhibitor 14 (FAK inhibitor) blocked the Robo4 knockdown-mediated alteration in glioma angiogenesis in vitro. Conclusion: Our results proved that Robo4 suppressed glioma-induced endothelial cell proliferation, migration and tube formation in vitro by inhibiting VEGR2-mediated activation of PI3K/AKT and FAK signaling pathways.

Adrenomedullin promotes human endothelial cell proliferation via HIF-1α

2012 ◽  
Vol 365 (1-2) ◽  
pp. 263-273 ◽  
Author(s):  
Li Chen ◽  
Ju-Hui Qiu ◽  
Ling-Ling Zhang ◽  
Xiang-Dong Luo
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cell ◽  
Human Endothelial Cell ◽  
Endothelial Cell Proliferation
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