scholarly journals Tricyclic antidepressant amitriptyline inhibits autophagic flux and prevents tube formation in vascular endothelial cells

2018 ◽  
Vol 124 (4) ◽  
pp. 370-384 ◽  
Author(s):  
Yinglu Guan ◽  
Xiang Li ◽  
Michihisa Umetani ◽  
Krishna M. Boini ◽  
Pin‐Lan Li ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Tube Formation ◽  
Tricyclic Antidepressant ◽  
Autophagic Flux ◽  
Vascular Endothelial

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 Tim-3 promotes tube formation and decreases tight junction formation in vascular endothelial cells

2020 ◽  
Vol 40 (10) ◽  
Author(s):  
Yizi Cong ◽  
Xingmiao Wang ◽  
Suxia Wang ◽  
Guangdong Qiao ◽  
Yalun Li ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Tight Junction ◽  
Immune Escape ◽  
Vascular Endothelial Cells ◽  
Tumour Progression ◽  
Umbilical Vein ◽  
Tube Formation ◽  
In Vitro Assays ◽  
Vegf Receptor ◽  
Vascular Endothelial

Abstract As a negative immune checkpoint molecule, T-cell immunoglobulin domain and mucin domain containing molecule-3 (Tim-3) has been found to serve a crucial role in immune escape and tumour progression. Previous studies have reported that Tim-3 is important to endothelial cells and it has also been demonstrated to be involved in numerous types of human diseases, including melanoma, lymphoma, rickettsial infection and atherosclerosis; however, its exact mechanism of action remains largely unknown. In the present study, Tim-3 was overexpressed in vascular endothelial human lung microvascular endothelial cells (HMVECs) and human umbilical vein endothelial cells (HUVECs), and in vitro assays were used to determine that Tim-3 promoted cell proliferation, migration, invasion and tube formation through activating cyclin D1 (CCND1), Ras homolog gene family member A and vascular endothelial growth factor (VEGF) receptor 2 (VEGFR2). Additionally, Tim-3 decreased tight junction (TJ) formation and the transepithelial resistance (TER) of endothelial cells by decreasing the expression levels of TJ protein 2, Occludin and claudin 1 (CLND1). In conclusion, these findings suggested that Tim-3 may exert a positive role in angiogenesis and a negative role in TJ formation in vascular endothelial cells, which may provide novel strategies for the treatment of Tim-3-associated diseases.

scholarly journals TRPM7 regulates vascular endothelial cell adhesion and tube formation

2015 ◽  
Vol 308 (4) ◽  
pp. C308-C318 ◽  
Author(s):  
Zhao Zeng ◽  
Koichi Inoue ◽  
Huawei Sun ◽  
Tiandong Leng ◽  
Xuechao Feng ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Transient Receptor Potential ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial Cell ◽  
Underlying Mechanism ◽  
Tube Formation ◽  
Vascular Endothelial ◽  
Cell Contractility ◽  
Transient Receptor Potential Melastatin

Transient receptor potential melastatin 7 (TRPM7) is a nonselective cation channel with an α-kinase domain in its COOH terminal, known to play a role in diverse physiological and pathological processes such as Mg2+ homeostasis, cell proliferation, and hypoxic neuronal injury. Increasing evidence suggests that TRPM7 contributes to the physiology/pathology of vascular systems. For example, we recently demonstrated that silencing TRPM7 promotes growth and proliferation and protects against hyperglycemia-induced injury in human umbilical vein endothelial cells (HUVECs). Here we investigated the potential effects of TRPM7 on morphology, adhesion, migration, and tube formation of vascular endothelial cells and the potential underlying mechanism. We showed that inhibition of TRPM7 function in HUVECs by silencing TRPM7 decreases the density of TRPM7-like current and cell surface area and inhibits cell adhesion to Matrigel. Silencing TRPM7 also promotes cell migration, wound healing, and tube formation. Further studies showed that the extracellular signal-regulated kinase (ERK) pathway is involved in the change of cell morphology and the increase in HUVEC migration induced by TRPM7 silencing. We also demonstrated that silencing TRPM7 enhances the phosphorylation of myosin light chain (MLC) in HUVECs, which might be involved in the enhancement of cell contractility and motility. Collectively, our data suggest that the TRPM7 channel negatively regulates the function of vascular endothelial cells. Further studies on the underlying mechanism may facilitate the development of the TRPM7 channel as a target for the therapeutic intervention of vascular diseases.

Inhibitory effect of methylmercury on migration and tube formation by cultured human vascular endothelial cells

1995 ◽  
Vol 69 (6) ◽  
pp. 357-361 ◽  
Author(s):  
Takuji Kishimoto ◽  
Tetsuhisa Oguri ◽  
Miyoko Abe ◽  
Hiroko Kajitani ◽  
Manabu Tada
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Inhibitory Effect ◽  
Tube Formation ◽  
Vascular Endothelial

Effects of glucose on migration, proliferation and tube formation by vascular endothelial cells

1991 ◽  
Vol 60 (1) ◽  
pp. 245-252 ◽  
Author(s):  
Junko N. Hayashi ◽  
Hideki Ito ◽  
Toshie Kanayasu ◽  
Noriko Asuwa ◽  
Ikuo Morita ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Tube Formation ◽  
Vascular Endothelial

scholarly journals Effects of nicardipine on tube formation of bovine vascular endothelial cells in vitro.

Stroke ◽  
1992 ◽  
Vol 23 (11) ◽  
pp. 1637-1642 ◽  
Author(s):  
T Kaneko ◽  
I Nagata ◽  
S Miyamoto ◽  
H Kubo ◽  
H Kikuchi ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Tube Formation ◽  
Vascular Endothelial
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