scholarly journals Effects of high glucose on human umbilical vein endothelial cell permeability and myosin light chain phosphorylation

2015 ◽  
Vol 7 (1) ◽  
Author(s):  
Xiao-Yan Zhao ◽  
Xiao-Fang Wang ◽  
Ling Li ◽  
Li Zhang ◽  
De-Liang Shen ◽  
...  
2019 ◽  
Vol 38 (6) ◽  
pp. 685-693 ◽  
Author(s):  
S Chen ◽  
J Ma ◽  
H Zhu ◽  
S Deng ◽  
M Gu ◽  
...  

High glucose (HG) induces vascular injury in diabetes. Hydroxysafflor yellow A (HSYA) has been used to ameliorate ischemic cardiovascular diseases in China for many years. In the present study, we assessed whether HSYA has a potential protective role in HG-induced human umbilical vein endothelial cell (HUVEC) injury. Cell viability was determined with an 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) assay. Cell apoptosis was detected by fluorescein isothiocyanate/propidium iodide staining assay. The endothelial cell permeability was measured with a permeability assay. Cell adhesion molecule (CAM) expression, vascular endothelial growth factor, and basic fibroblast growth factor levels were detected with an enzyme-linked immunosorbent assay. Reactive oxygen species (ROS) formation was measured with a DCF-DA assay. Protein expression of NADPH oxidase 4 (NOX4) was measured by Western blotting. Our data indicated that HG increases HUVEC apoptosis, vascular permeability, monocyte adhesion, the level of CAMs, the formation of ROS, and NOX4 expression. Our data revealed that HG increases vascular injury, which is attenuated by HSYA. Because vascular inflammation has a key role in the development of diabetes mellitus, our results implied that HSYA is considered as a potential agent for diabetic vascular injury treatment.


2004 ◽  
Vol 287 (5) ◽  
pp. L911-L918 ◽  
Author(s):  
Talaibek Borbiev ◽  
Anna Birukova ◽  
Feng Liu ◽  
Saule Nurmukhambetova ◽  
William T. Gerthoffer ◽  
...  

We have previously shown that thrombin induces endothelial cell barrier dysfunction via cytoskeleton activation and contraction and have determined the important role of endothelial cell myosin light chain kinase (MLCK) in this process. In the present study we explored p38 MAP kinase as a potentially important enzyme in thrombin-mediated endothelial cell contractile response and permeability. Thrombin induces significant p38 MAP kinase activation in a time-dependent manner with maximal effect at 30 min, which correlates with increased phosphorylation of actin- and myosin-binding protein, caldesmon. Both SB-203580 and dominant negative p38 adenoviral vector significantly attenuated thrombin-induced declines in transendothelial electrical resistance. Consistent with these data SB-203580 decreased actin stress fiber formation produced by thrombin in endothelium. In addition, dominant negative p38 had no effect on thrombin-induced myosin light chain diphosphorylation. Thrombin-induced total and site-specific caldesmon phosphorylation (Ser789) as well as dissociation of caldesmon-myosin complex were attenuated by SB-203580 pretreatment. These results suggest the involvement of p38 MAP kinase activities and caldesmon phosphorylation in the MLCK-independent regulation of thrombin-induced endothelial cell permeability.


2017 ◽  
Vol 102 (3) ◽  
pp. 377-383 ◽  
Author(s):  
Chun-Hong Yu ◽  
Suriguga ◽  
Meng Gong ◽  
Wen-Juan Liu ◽  
Ning-Xuan Cui ◽  
...  

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