scholarly journals A Heterodimeric Cytokine, Consisting of IL-17A and IL-17F, Promotes Migration and Capillary-Like Tube Formation of Human Vascular Endothelial Cells

2016 ◽  
Vol 240 (1) ◽  
pp. 47-56 ◽  
Author(s):  
Muneo Numasaki ◽  
Hiroki Tsukamoto ◽  
Yoshihisa Tomioka ◽  
Yasuhiko Nishioka ◽  
Takashi Ohrui
2018 ◽  
Vol 124 (4) ◽  
pp. 370-384 ◽  
Author(s):  
Yinglu Guan ◽  
Xiang Li ◽  
Michihisa Umetani ◽  
Krishna M. Boini ◽  
Pin‐Lan Li ◽  
...  

Blood ◽  
2010 ◽  
Vol 115 (20) ◽  
pp. 4130-4137 ◽  
Author(s):  
Jinmin Gao ◽  
Lei Sun ◽  
Lihong Huo ◽  
Min Liu ◽  
Dengwen Li ◽  
...  

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.


2020 ◽  
Vol 40 (10) ◽  
Author(s):  
Yizi Cong ◽  
Xingmiao Wang ◽  
Suxia Wang ◽  
Guangdong Qiao ◽  
Yalun Li ◽  
...  

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.


2015 ◽  
Vol 308 (4) ◽  
pp. C308-C318 ◽  
Author(s):  
Zhao Zeng ◽  
Koichi Inoue ◽  
Huawei Sun ◽  
Tiandong Leng ◽  
Xuechao Feng ◽  
...  

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.


1995 ◽  
Vol 69 (6) ◽  
pp. 357-361 ◽  
Author(s):  
Takuji Kishimoto ◽  
Tetsuhisa Oguri ◽  
Miyoko Abe ◽  
Hiroko Kajitani ◽  
Manabu Tada

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

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

2018 ◽  
Vol 59 (5) ◽  
pp. 1086-1095 ◽  
Author(s):  
Chaofeng Miao ◽  
Haixia Cao ◽  
Yonggan Zhang ◽  
Xueli Guo ◽  
Zifan Wang ◽  
...  

1995 ◽  
Vol 69 (10) ◽  
pp. 718-721 ◽  
Author(s):  
Takuji Kishimoto ◽  
Tetsuhisa Oguri ◽  
Daizo Ueda ◽  
Manabu Tada

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