scholarly journals Paracrine Release from Nonviral Engineered Adipose-Derived Stem Cells Promotes Endothelial Cell Survival and Migration In Vitro

2013 ◽  
Vol 22 (3) ◽  
pp. 483-491 ◽  
Author(s):  
Lorenzo Deveza ◽  
Jeffrey Choi ◽  
Galym Imanbayev ◽  
Fan Yang
Keyword(s):  
Stem Cells ◽  
Endothelial Cell ◽  
Cell Survival ◽  
Adipose Derived Stem Cells ◽  
Endothelial Cell Survival ◽  
And Migration

Enhancement on Primate Corneal Endothelial Cell Survival In Vitro by a ROCK Inhibitor

2009 ◽  
Vol 50 (8) ◽  
pp. 3680 ◽  
Author(s):  
Naoki Okumura ◽  
Morio Ueno ◽  
Noriko Koizumi ◽  
Yuji Sakamoto ◽  
Kana Hirata ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Survival ◽  
Corneal Endothelial Cell ◽  
Rock Inhibitor ◽  
Endothelial Cell Survival

Neuropilin-2 interacts with VEGFR-2 and VEGFR-3 and promotes human endothelial cell survival and migration

Blood ◽  
2006 ◽  
Vol 108 (4) ◽  
pp. 1243-1250 ◽  
Author(s):  
Benoit Favier ◽  
Antoine Alam ◽  
Pauline Barron ◽  
Jacques Bonnin ◽  
Patricia Laboudie ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Survival ◽  
Endothelial Cell Migration ◽  
Human Endothelial Cell ◽  
Human Endothelial Cells ◽  
Endothelial Cell Survival ◽  
Biological Responses ◽  
And Migration ◽  
Endothelial Growth Factor

Abstract Neuropilin 2 (NRP2) is a receptor for the vascular endothelial growth factor (VEGF) and the semaphorin (SEMA) families, 2 unrelated ligand families involved in angiogenesis and neuronal guidance. NRP2 specifically binds VEGF-A and VEGF-C, although the biological relevance of these interactions in human endothelial cells is poorly understood. In this study, we show that both VEGF-A and VEGF-C induce the interaction of NRP2 with VEGFR-2. This interaction correlated with an enhancement of the VEGFR-2 phosphorylation threshold. Overexpression of NRP2 in primary human endothelial cells promoted cell survival induced by VEGF-A and VEGF-C. In contrast, SEMA3F, another ligand for NRP2, was able to inhibit human endothelial cell survival and migration induced by VEGF-A and VEGF-C. Moreover, a siRNA targeting specifically NRP2 was a potent inhibitor of human endothelial cell migration induced by VEGF-A and VEGF-C. Thus, our data indicate that NRP2 acts as a coreceptor that enhances human endothelial cell biological responses induced by VEGF-A and VEGF-C.

The effects of various growth factors on endothelial cell survival in vitro

1989 ◽  
Vol 162 (3) ◽  
pp. 1010-1016 ◽  
Author(s):  
Takafumi Etoh ◽  
Kazuhiko Takehara ◽  
Atsuyuki Igarashi ◽  
Yasumasa Ishibashi
Keyword(s):  
Growth Factors ◽  
Endothelial Cell ◽  
Cell Survival ◽  
Endothelial Cell Survival

Signaling and regulation of endothelial cell survival by angiopoietin-2

2006 ◽  
Vol 291 (4) ◽  
pp. H1635-H1645 ◽  
Author(s):  
Rania Harfouche ◽  
Sabah N. A. Hussain
Keyword(s):  
Cell Migration ◽  
Endothelial Cell ◽  
Cell Survival ◽  
Umbilical Vein ◽  
Biological Effects ◽  
Pi3 Kinase ◽  
Endothelial Cell Migration ◽  
Endothelial Cell Survival ◽  
Induced Apoptosis

Angiopoietins are ligands for endothelial cell-specific Tie-2 receptors. Whereas angiopoietin-1 (Ang-1) activates these receptors and promotes cell survival, migration, and sprouting, little information is available regarding how Ang-2 influences these cells. In this study, we evaluated signaling pathways and biological effects of physiological concentrations of Ang-2 in cultured human umbilical vein endothelial cells. Ang-2 at 150 and 300 ng/ml elicited a transient (reaching peak values within 15 min of exposure) increase in the phosphorylation of Tie-2 receptors, protein kinase B (Akt), ERK1/2, and p38 members of the mitogen-activated protein kinases. However, unlike Ang-1, Ang-2 significantly inhibited JNK/SAPK phosphorylation. When vascular endothelial growth factor (VEGF) was present along with Ang-2, ERK1/2 phosphorylation was inhibited, whereas augmentation of Ang-1-induced ERK1/2 phosphorylation was triggered by VEGF. Ang-2 treatment had no effect on cell migration and in vitro wound healing but significantly attenuated serum deprivation-induced apoptosis and promoted survival. These effects were completely reversed by phosphatidylinositol 3 (PI3)-kinase and ERK1/2 inhibitors but were augmented by an inhibitor of the p38 pathway. These results suggest that Ang-2 promotes endothelial cell survival through the ERK1/2 and PI3-kinase pathways and that this angiopoietin is not a strong promoter of endothelial cell migration. We also conclude that the nature of interactions in terms of ERK1/2 activation between Ang-2 and VEGF is different from that of Ang-1 and VEGF.

The effects of scleroderma sera on endothelial cell survival in vitro

1990 ◽  
Vol 282 (8) ◽  
pp. 516-519 ◽  
Author(s):  
T. Etoh ◽  
A. Igarashi ◽  
K. Iozumi ◽  
Y. Ishibashi ◽  
K. Takehara
Keyword(s):  
Endothelial Cell ◽  
Cell Survival ◽  
Endothelial Cell Survival

scholarly journals Donor-dependent variances of human adipose-derived stem cells in respect to the in-vitro endothelial cell differentiation capability

Adipocyte ◽  
2017 ◽  
Vol 6 (1) ◽  
pp. 20-32 ◽  
Author(s):  
Jascha Ell ◽  
Sybille Regn ◽  
Anna-Maria Buchberger ◽  
Achim von Bomhard ◽  
Thomas Stark ◽  
...  
Keyword(s):  
Stem Cells ◽  
Endothelial Cell ◽  
Cell Differentiation ◽  
Adipose Derived Stem Cells ◽  
Endothelial Cell Differentiation

scholarly journals Effects mediated by the α7 nicotinic acetylcholine receptor on cell proliferation and migration in rat adipose-derived stem cells

2020 ◽  
Vol 64 (s2) ◽  
Author(s):  
Marta Pernarella ◽  
Roberta Piovesana ◽  
Carlo Matera ◽  
Alessandro Faroni ◽  
Mario Fiore ◽  
...  
Keyword(s):  
Stem Cells ◽  
Nicotinic Receptors ◽  
Adipose Derived Stem Cells ◽  
Α7 Nicotinic Acetylcholine Receptor ◽  
Differentiation Potential ◽  
Physiological Processes ◽  
Α7 Nachr ◽  
And Migration ◽  
Proliferation And Migration

Adipose-derived stem cells (ASCs) are an attractive source for regenerative medicine as they can be easily isolated, rapidly expandable in culture and show excellent in vitro differentiation potential. Acetylcholine (ACh), one of the main neurotransmitters in central and peripheral nervous systems, plays key roles in the control of several physiological processes also in non-neural tissues. As demonstrated in our previous studies, ACh can contribute to the rat ASCs physiology, negatively modulating ASCs proliferation and migration via M2 muscarinic receptor (mAChR) activation. In the present work we show that rat ASCs also express α7 nicotinic receptors (nAChRs). In particular, we have investigated the effects mediated by the selective activation of α7 nAChRs, which causes a reduction of ASC proliferation without affecting cell survival and morphology, and significantly promotes cell migration via upregulation of the CXCR4 expression. Interestingly, the activation of the α7 nAChR also upregulates the expression of M2 mAChR protein, indicating a cooperation between muscarinic and nicotinic receptors in the inhibition of ASC proliferation.  

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