Cryptotanshinone and wogonin up-regulate eNOS in vascular endothelial cells via ERα and down-regulate iNOS in LPS stimulated vascular smooth muscle cells via ERβ

2015 ◽  
Vol 39 (2) ◽  
pp. 249-258 ◽  
Author(s):  
Barnabas Oche ◽  
Lu Chen ◽  
Ya-ke Ma ◽  
Yue Yang ◽  
Chun-xiao Li ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Vascular Endothelial Cells ◽  
Muscle Cells ◽  
Vascular Endothelial

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.

scholarly journals Long Non-Coding RNAs in Cardiac Remodeling

2017 ◽  
Vol 41 (5) ◽  
pp. 1830-1837 ◽  
Author(s):  
Shutong Shen ◽  
Huimin Jiang ◽  
Yihua Bei ◽  
Junjie Xiao ◽  
Xinli Li
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Cardiac Remodeling ◽  
Vascular Endothelial Cells ◽  
Muscle Cells ◽  
Vascular Endothelial ◽  
Non Coding Rnas

Cardiac remodeling occurs after stress to the heart, manifested as pathological processes, including hypertrophy and apoptosis of cardiomyocytes, dysfunction of vascular endothelial cells and vascular smooth muscle cells as well as differentiation and proliferation of fibroblasts, ultimately resulting in progression of cardiovascular diseases. Emerging evidence has revealed that long non-coding RNAs (lncRNAs) acted as powerful and dynamic modifiers of cardiac remodeling. LncRNAs including Chaer, Chast, Mhrt, CHRF, ROR, H19, and MIAT have been implicated in cardiac hypertrophy while NRF, H19, APF, CARL, UCA, Mhrt and several other lncRNAs (n379599, n379519, n384640, n380433 and n410105) in cardiomyocyte loss and extracellular matrix remodeling. In addition, MALAT1 and TGFB2-OT1 have been reported to contribute to vascular endothelial cells dysfunction while lincRNA-p21 and lnc-Ang362 to vascular smooth muscle cells proliferation. Thus, manipulation of lncRNA expression levels through either the inhibition of disease-up-regulated lncRNAs or increasing disease-down-regulated lncRNAs represents novel therapeutic strategies for cardiac remodeling.

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