DARC Regulates Angiogenesis by Mediating Vascular Endothelial Cell Migration

2020 ◽  
Author(s):  
Xiaolin Wang ◽  
Yongqian Bian ◽  
Yuejun Li ◽  
Jing Li ◽  
Congying Zhao ◽  
...  
Keyword(s):  
Cell Migration ◽  
Endothelial Cell ◽  
Vascular Endothelial Cell ◽  
Tube Formation ◽  
Endothelial Cell Migration ◽  
Immunofluorescent Staining ◽  
Control Group ◽  
Rhoa Activation ◽  
And Control

Abstract Background: DARC (The Duffy antigen receptor for chemokines) is a kind of glycosylated membrane protein that binds to members of the CXC chemokine family associated with angiogenesis and has recently been reported to be implicated in diverse normal physiologic processes. This study aimed to investigate the involvement of DARC in angiogenesis, which is known to generate new capillary blood vessels from preexisting ones. Methods: HDMECs (Human dermal microvascular endothelial cells) were divided into two groups (DARC overexpression group, and control group). We used Brdu staining to detect cell proliferation, and wound healing assay to detect cell migration. Then tube formation assay were observed. Also, western blot and immunofluorescent staining were used to estimate the relationship between DARC and RhoA (Ras homolog gene family, member A). Results: HDMECs proliferation, migration, and tube formation were inhibited significantly when DARC was overexpressed intracellular. DARC impaired microfilament dynamics and intercellular connection in migrating cells, and RhoA activation underlay the effect of DARC on endothelial cell. Furthermore, DARC inhibited the formation of new capillaries in vitro. Conclusion: Our findings revealed the role of DARC in the angiogenic process and provided a novel mechanism for RhoA activation during endothelial cell migration and angiogenesis.

CYLD regulates angiogenesis by mediating vascular endothelial cell migration

Blood ◽  
2010 ◽  
Vol 115 (20) ◽  
pp. 4130-4137 ◽  
Author(s):  
Jinmin Gao ◽  
Lei Sun ◽  
Lihong Huo ◽  
Min Liu ◽  
Dengwen Li ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Migration ◽  
Endothelial Cell ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial Cell ◽  
Tube Formation ◽  
Endothelial Cell Migration ◽  
Vascular Endothelial

Cylindromatosis (CYLD) is a deubiquitinase that was initially identified as a tumor suppressor and has recently been implicated in diverse normal physiologic processes. In this study, we have investigated the involvement of CYLD in angiogenesis, the formation of new blood vessels from preexisting ones. We find that knockdown of CYLD expression significantly impairs angiogenesis in vitro in both matrigel-based tube formation assay and collagen-based 3-dimensional capillary sprouting assay. Disruption of CYLD also remarkably inhibits angiogenic response in vivo, as evidenced by diminished blood vessel growth into the angioreactors implanted in mice. Mechanistic studies show that CYLD regulates angiogenesis by mediating the spreading and migration of vascular endothelial cells. Silencing of CYLD dramatically decreases microtubule dynamics in endothelial cells and inhibits endothelial cell migration by blocking the polarization process. Furthermore, we identify Rac1 activation as an important factor contributing to the action of CYLD in regulating endothelial cell migration and angiogenesis. Our findings thus uncover a previously unrecognized role for CYLD in the angiogenic process and provide a novel mechanism for Rac1 activation during endothelial cell migration and angiogenesis.

Cyclic strain-mediated regulation of vascular endothelial cell migration and tube formation

2005 ◽  
Vol 329 (2) ◽  
pp. 573-582 ◽  
Author(s):  
Nicholas Von Offenberg Sweeney ◽  
Philip M. Cummins ◽  
Eoin J. Cotter ◽  
Paul A. Fitzpatrick ◽  
Yvonne A. Birney ◽  
...  
Keyword(s):  
Cell Migration ◽  
Endothelial Cell ◽  
Vascular Endothelial Cell ◽  
Cyclic Strain ◽  
Tube Formation ◽  
Endothelial Cell Migration ◽  
Vascular Endothelial

Functionally defining the endothelial transcriptome, from Robo4 to ECSCR

2009 ◽  
Vol 37 (6) ◽  
pp. 1214-1217 ◽  
Author(s):  
Ana Raquel Verissimo ◽  
John M.J. Herbert ◽  
Victoria L. Heath ◽  
John A. Legg ◽  
Helen Sheldon ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Migration ◽  
Endothelial Cell ◽  
Critical Role ◽  
Tube Formation ◽  
Endothelial Cell Migration ◽  
In Vitro Assays ◽  
Filamin A ◽  
Interfering Rna

We have applied search algorithms to expression databases to identify genes whose expression is restricted to the endothelial cell. Such genes frequently play a critical role in endothelial biology and angiogenesis. Two such genes are the roundabout receptor Robo4 and the ECSCR (endothelial-cell-specific chemotaxis regulator). Endothelial cells express both Robo1 and Robo4, which we have knocked down using siRNA (small interfering RNA) and then studied the effect in a variety of in vitro assays. Both Robo4 and Robo1 knockdown inhibited in vitro tube formation on Matrigel™. Transfection of Robo4 into endothelial cells increased the number of filopodial extensions from the cell, but failed to do so in Robo1-knockdown cells. Separate immunoprecipitation studies showed that Robo1 and Robo4 heterodimerize. We conclude from this and other work that a heteroduplex of Robo1 and Robo4 signals through WASP (Wiskott–Aldrich syndrome protein) and other actin nucleation-promoting factors to increase the number of filopodia and cell migration. Knockdown of the transmembrane ECSCR protein in endothelial cells also reduced chemotaxis and impaired tube formation on Matrigel™. Yeast two-hybrid analysis and immunoprecipitation studies showed that, in contrast with the roundabouts, ECSCR binds to the actin-modulatory filamin A. We conclude that all three of these genes are critical for effective endothelial cell migration and, in turn, angiogenesis.

scholarly journals P10 MIR-133a overexpression impairs endothelial cell migration and tube formation in vitro

2018 ◽  
Author(s):  
Sathishkumar Kurusamy ◽  
Jude C Ihugba ◽  
Angel L Armesilla ◽  
James M Cotton
Keyword(s):  
Cell Migration ◽  
Endothelial Cell ◽  
Tube Formation ◽  
Endothelial Cell Migration

scholarly journals Ablation of SGK1 Impairs Endothelial Cell Migration and Tube Formation Leading to Decreased Neo-Angiogenesis Following Myocardial Infarction

PLoS ONE ◽  
2013 ◽  
Vol 8 (11) ◽  
pp. e80268 ◽  
Author(s):  
Elham Zarrinpashneh ◽  
Tommaso Poggioli ◽  
Padmini Sarathchandra ◽  
Jonas Lexow ◽  
Laurent Monassier ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cell Migration ◽  
Endothelial Cell ◽  
Tube Formation ◽  
Endothelial Cell Migration
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