2015
DOI: 10.1016/j.ceb.2015.07.009
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The same but different: signaling pathways in control of endothelial cell migration

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Cited by 25 publications
(18 citation statements)
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“…In a landmark study, Xu et al ( 2014 ) showed that regenerating vessels in the regenerating tail fin originate from vein-derived cells that acquire angiogenic potential. These cells migrate singly or collectively and organize into vessel in response to chemokine signaling (reviewed by Hasan and Siekmann, 2015 ). However, the applicability of this model to the study of vascular regeneration could be much more widely exploited.…”
Section: Zebrafish As a Model For Angiogenesis Researchmentioning
confidence: 99%
“…In a landmark study, Xu et al ( 2014 ) showed that regenerating vessels in the regenerating tail fin originate from vein-derived cells that acquire angiogenic potential. These cells migrate singly or collectively and organize into vessel in response to chemokine signaling (reviewed by Hasan and Siekmann, 2015 ). However, the applicability of this model to the study of vascular regeneration could be much more widely exploited.…”
Section: Zebrafish As a Model For Angiogenesis Researchmentioning
confidence: 99%
“…The emergence of these sprouts is guided by several factors (reviewed in Hasan and Siekmann, 2015), including attractive signals (e.g. Vegf-A) and repulsive signals (e.g.…”
Section: Tip Cell Selection and Functionmentioning
confidence: 99%
“…Thirdly, VEGF-induced Rac1 activation in ECs is mainly mediated by Vav2 phosphorylation 28 , while so far there is no evidence showing that DOCK180 is directly stimulated by VEGF in mammalian cells. Moreover, DOCK180 deficiency results in vascular defects but has no impact on VEGF-induced EC migration (reviewed in) 8 , further supporting that DOCK180 is not directly linked to VEGFR signalling. Taken these together, we propose that stimulation of the DOCK180 pathway by PTP1B inhibitor, which does not require concomitant VEGFR2 activation as a prerequisite, may represent an important alternative mechanism of PTP1B inhibitor-stimulated EC motility (see Supplementary Fig.…”
Section: Discussionmentioning
confidence: 94%
“…Increased EC migration is also favourable for re-endothelialization of the denuded luminal surface of injured blood vessels, which is critical to prevent the development of intimal hyperplasia and stenosis following mechanical vessel injuries 4 5 . EC migration is coordinated by complex signalling mechanisms, of which those mediated by vascular endothelial growth factor receptors (VEGFRs) and the Rho family small GTPases have critical roles 6 7 8 . VEGF is one of the most important chemotactic factors that guide the directional movement of endothelial cells 6 .…”
mentioning
confidence: 99%