Endothelial Cell Regulation of Vascular Smooth Muscle

1989 ◽  
pp. 755-771 ◽  
Author(s):  
Robert F. Highsmith ◽  
Oliver M. FitzGerald
Keyword(s):  
Smooth Muscle ◽  
Endothelial Cell ◽  
Vascular Smooth Muscle ◽  
Cell Regulation

Inhibition of vascular smooth muscle and endothelial cell migration by apolipoprotein J

2000 ◽  
Vol 191 (4) ◽  
pp. S2
Author(s):  
Nayan Sivamurthy ◽  
Darren I Rohan ◽  
David H Stone ◽  
William C Quist ◽  
Frank W LoGerfo
Keyword(s):  
Smooth Muscle ◽  
Cell Migration ◽  
Endothelial Cell ◽  
Vascular Smooth Muscle ◽  
Endothelial Cell Migration ◽  
Apolipoprotein J

scholarly journals Vascular smooth muscle cell effect on endothelial cell endothelin-1 production

2000 ◽  
Vol 31 (4) ◽  
pp. 781-789 ◽  
Author(s):  
Gabriele Di Luozzo ◽  
Jaya Bhargava ◽  
Richard J. Powell
Keyword(s):  
Smooth Muscle ◽  
Endothelial Cell ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Endothelin 1

Divergent effects of 17-β-estradiol on human vascular smooth muscle and endothelial cell function diminishes TNF-α-induced neointima formation

2012 ◽  
Vol 420 (4) ◽  
pp. 828-833 ◽  
Author(s):  
Rungrat Nintasen ◽  
Kirsten Riches ◽  
Romana S. Mughal ◽  
Parnpen Viriyavejakul ◽  
Urai Chaisri ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Endothelial Cell ◽  
Vascular Smooth Muscle ◽  
Cell Function ◽  
Neointima Formation ◽  
Endothelial Cell Function ◽  
Tnf Α

The endothelial cell

2017 ◽  
Author(s):  
Ingrid Fleming ◽  
Brenda R. Kwak ◽  
Merlijn J. Meens
Keyword(s):  
Smooth Muscle ◽  
Endothelial Cell ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Blood Vessels ◽  
Vascular Smooth Muscle Cells ◽  
Vascular Endothelium ◽  
Structural Heterogeneity ◽  
Physical Barrier ◽  
Physiological Functions

The endothelium, a monolayer of cells that lines blood vessels, acts as a physical barrier between circulating blood and vascular smooth muscle cells. The purpose of this chapter is to provide a general overview on the structural heterogeneity of the endothelium. Moreover, the most important physiological functions of the vascular endothelium in blood vessels are discussed. More detailed insights into the pathogenesis of specific diseases, including atherosclerosis and hypertension, are provided in other chapters of this book.

TMEM98, a novel secretory protein, promotes endothelial cell adhesion as well as vascular smooth muscle cell proliferation and migration

2020 ◽  
Author(s):  
Mei Li ◽  
Hongmei Zhu ◽  
Xiaoyan Hu ◽  
Fuhua Gao ◽  
Xinxin Hu ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Endothelial Cell ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Transmembrane Protein ◽  
Vsmc Proliferation ◽  
And Migration ◽  
Proliferation And Migration

Transmembrane protein 98 (TMEM98) is a novel gene. In a prior study, we have shown that siRNA-mediated knockdown of TMEM98 inhibited interleukin (IL)-8-promoted endothelial cell (EC) adhesion as well as vascular smooth muscle cell (VSMC) proliferation and migration in the vascular endothelial and smooth muscle cells dysfunction. Herein, we used gain- and loss-of-function approaches combined with biochemical techniques to further explore the role of TMEM98 in the vascular wall cell. The expression and secretion of TMEM98 was increased in cultured human umbilical vein endothelial cells (HUVECs) and VSMCs treated with IL-8 and platelet-derived growth factor (PDGF)-BB. Also, PDGF-BB secretion was increased in TMEM98-treated HUVECs and VSMCs. Thus, it appears that TMEM98 and PDGF-BB form a positive feedback loop in potentiation of EC adhesion as well as VSMC proliferation and migration. Knockdown of TMEM98 mediated by siRNA inhibited PDGF-BB-promoted EC adhesion by downregulating the expression of ICAM-1 and VCAM-1 as well as impaired the proliferation and migration of VSMCs through suppressing the AKT/GSK3β/cyclin D1 signaling pathway and reducing the expression of β-catenin. Hence, TMEM98 promoted EC adhesion through inducing the expression of ICAM-1/VCAM-1 and triggered VSMC proliferation and migration through activating the ERK and AKT/GSK3β signaling pathways. Taken together, TMEM98 may serve as a potential therapeutic target for the clinical treatment.

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