Effects of herb therapy for benefiting qi and removing blood stasis on ultrastructure of vascular endothelial cells and vascular smooth muscle cells of uterine endometrium in rabbits with copper intrauterine device

2006 ◽  
Vol 4 (1) ◽  
pp. 60-63 ◽  
Author(s):  
Lei Lei
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Vascular Endothelial Cells ◽  
Intrauterine Device ◽  
Blood Stasis ◽  
Vascular Endothelial ◽  
Uterine Endometrium ◽  
Copper Intrauterine Device

Compared Study of Vascular Cell Response to Mg-Zn-Y-Nd and WE43 as Biodegradable Stents

2014 ◽  
Vol 915-916 ◽  
pp. 962-967 ◽  
Author(s):  
Xiao Li Liu ◽  
Ting Fei Xi ◽  
Yu Dong Zheng ◽  
Shao Kang Guan
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Vascular Endothelial Cells ◽  
Muscle Cells ◽  
Vascular Endothelial ◽  
Biodegradable Stents ◽  
No Release

To evaluate biocompatibility of Mg-Zn-Y-Nd alloy as vascular stent material, its influence on cytotoxicity, cell migration, cell chemotaxis and NO release of vascular endothelial cells and vascular smooth muscle cells were tested compared with WE43 alloy. Results show that Mg-Zn-Y-Nd alloy degraded slower and exhibited better cell viability and NO release than WE43; WE43 showed more significant effect on stimulating endothelial cells migration; Both alloys showed nonsignificant effect on vascular smooth muscle cells migration and chemotaxis. Mg-Zn-Y-Nd alloy exhibited great biocompatibility to vascular cells.

Aldosterone mediates its rapid effects in vascular endothelial cells through GPER activation

2013 ◽  
Vol 304 (6) ◽  
pp. C532-C540 ◽  
Author(s):  
Robert Gros ◽  
Qingming Ding ◽  
Bonan Liu ◽  
Jozef Chorazyczewski ◽  
Ross D. Feldman
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Cell Growth ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Mineralocorticoid Receptor ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Erk Phosphorylation

The importance of the rapid vascular effects of aldosterone is increasingly appreciated. Through these rapid pathways, aldosterone has been shown to regulate vascular contractility, cell growth, and apoptosis. In our most recent studies, we demonstrated the effects of aldosterone on cell growth and contractility in vascular smooth muscle cells. We showed that these effects could occur via activation of the classic mineralocorticoid receptor, as well the recently characterized G protein-coupled estrogen receptor (GPER), initially characterized as an estrogen-specific receptor. However, the mechanisms underlying aldosterone's endothelium-dependent actions are unknown. Furthermore, the ERK regulatory and proapoptotic effects of aldosterone mediated by GPER activation in cultured vascular smooth muscle cells were only apparent when GPER was reintroduced into these cells by gene transfer. Whether GPER activation via aldosterone might be an important regulator in native vascular cells has been questioned. Therefore, to determine the role of GPER in mediating aldosterone's effects on cell growth and vascular reactivity in native cells, we examined rat aortic vascular endothelial cells, a model characterized by persistent robust expression of GPER, but without detectable mineralocorticoid receptor expression. In these endothelial cells, the GPER agonist G1 mediates a rapid increase in ERK phosphorylation that is wholly GPER-dependent, paralleling the actions of aldosterone. The effects of G1 and aldosterone to stimulate ERK phosphorylation paralleled their proapoptotic and antiproliferative effects. In previous studies, we reported that aldosterone mediates a rapid endothelium-dependent vasodilatory effect, antagonistic to its direct vasoconstrictor effect in endothelium-denuded preparations. Using a rat aortic ring/organ bath preparation to determine the GPER dependence of aldosterone's endothelium-dependent vasodilator effects, we demonstrate that aldosterone inhibits phenylephrine-mediated contraction. This vasodilator effect parallels the actions of the GPER agonist G1. Furthermore, the effects of aldosterone were completely ablated by the GPER antagonist G15. These data support an important role of GPER activation in aldosterone-mediated regulation of endothelial cell growth, as well as in aldosterone's endothelium-mediated regulation of vasoreactivity.

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