Id1-induced inhibition of p53 facilitates endothelial cell migration and tube formation by regulating the expression of beta1-integrin

2011 ◽  
Vol 357 (1-2) ◽  
pp. 125-133 ◽  
Author(s):  
Juhui Qiu ◽  
Guixue Wang ◽  
Jianjun Hu ◽  
Qin Peng ◽  
Yiming Zheng
Keyword(s):  
Cell Migration ◽  
Endothelial Cell ◽  
Tube Formation ◽  
Endothelial Cell Migration ◽  
Beta1 Integrin

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

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

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.

P736Histone marks induced by the methyltransferase SETD7 modulate angiogenic response in diabetes

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
S A Mohammed ◽  
S Costantino ◽  
A Akhmedov ◽  
S Ambrosini ◽  
G Karsay ◽  
...  
Keyword(s):  
Cell Migration ◽  
Endothelial Cell ◽  
Tube Formation ◽  
Endothelial Cell Migration ◽  
Rna Seq ◽  
Hindlimb Ischemia ◽  
Angiogenic Response ◽  
Pharmacological Blockade ◽  
Type 2 Diabetic

Abstract Introduction Despite advances in revascularization strategies, type 2 diabetic (T2D) patients with peripheral artery disease (PAD) continue to have a high risk of limb amputation. Hence, strategies that promote vascularization can be considered as a novel therapeutic option in T2D patients with PAD. Epigenetic modifications of histones and DNA have emerged as key modulators of gene expression. Mono-methylation of histone 3 at lysine 4 (H3K4m1) – a specific epigenetic signature induced by the methyltransferase SETD7 – favours a chromatin conformation enabling the transcription of genes involved in inflammation and oxidative stress. Purpose To investigate whether SETD7 modulates angiogenesis in experimental diabetes. Methods Human aortic endothelial cells (HAECs) were cultured in growth factor-free medium and exposed either to normal glucose (NG, 5 mM) or high glucose (HG, 25 mM) for 48 hours. SETD7 protein and H3K4me1 levels were investigated by Western blot and chromatin immunoprecipitation (ChIP). Knockdown of SETD7 was achieved by small interfering RNA (siRNA). Pharmacological blockade of SETD7 was performed by using the highly selective inhibitor (R)-PFI-2, while its inactive enantiomer, (S)-PFI-2, was used as a control. Scratch and tube formation assays were performed to investigate the impact of SETD7 on angiogenic properties of HAECs. RNA sequencing (RNA-seq) and Ingenuity Pathway Analysis (IPA) were employed to unveil putative genes regulated by SETD7 in HG-treated HAECs. SETD7 expression was also investigated in muscular specimens isolated from type 2 diabetic (db/db) mice and non-diabetic mice undergoing hindlimb ischemia for 21 days. Results HG exposure in HAECs led to a time-dependent increase of both SETD7 gene and protein expression, as compared to NG. SETD7 upregulation in HG-treated HAECs was associated with an increase of H3K4me1 levels as well as with impaired endothelial cell migration and tube formation. Of interest, both gene silencing and pharmacological blockade of SETD7 rescued hyperglycemia-induced impairment of angiogenic properties in HAECs. RNA-seq in HG-treated HAECs with and without SETD7 depletion unveiled an array of differentially expressed genes, which were mainly involved in blood vessel growth and angiogenic response, as assessed by IPA analysis. Among dysregulated genes, ChIP assays showed that SETD7-dependent chromatin changes enabled the transcription of Semaphorin 3G (SEMA-3G), a negative regulator of endothelial cell migration. Indeed, gene silencing of SETD7 blunted SEMA-3G expression in HAECs exposed to HG. Consistent with our in vitro observations, SETD7 was upregulated in adductor muscle specimens from db/db mice undergoing hindlimb ischemia as compared to non-diabetic animals. Conclusions Pharmacological blockade of SETD7 by (R)-PFI-2 may represent a potential therapeutic approach to boost post-ischemic vascularization in T2D patients with PAD.

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.

scholarly journals Anti-angiogenic effect of arsenic trioxide in lung cancer via inhibition of endothelial cell migration, proliferation and tube formation

2017 ◽  
Vol 14 (3) ◽  
pp. 3103-3109 ◽  
Author(s):  
Meng-Hang Yang ◽  
Ke-Jie Chang ◽  
Jin-Cheng Zheng ◽  
Hai Huang ◽  
Guang-Yuan Sun ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Migration ◽  
Endothelial Cell ◽  
Arsenic Trioxide ◽  
Tube Formation ◽  
Endothelial Cell Migration ◽  
Angiogenic Effect
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