Shear Stress-induced NO Production Model of Vascular Endothelial Cell

2016 ◽  
Vol 136 (2) ◽  
pp. 116-122
Author(s):  
Yuji Ohashi ◽  
Yoichi Yamazaki ◽  
Yoshimi Kamiyama
1986 ◽  
Vol 83 (7) ◽  
pp. 2114-2117 ◽  
Author(s):  
P. F. Davies ◽  
A. Remuzzi ◽  
E. J. Gordon ◽  
C. F. Dewey ◽  
M. A. Gimbrone

2013 ◽  
Vol 7 (6) ◽  
pp. 472-478 ◽  
Author(s):  
Xianliang Huang ◽  
Yang Shen ◽  
Yi Zhang ◽  
Lin Wei ◽  
Yi Lai ◽  
...  

1991 ◽  
Vol 113 (2) ◽  
pp. 123-131 ◽  
Author(s):  
G. Helmlinger ◽  
R. V. Geiger ◽  
S. Schreck ◽  
R. M. Nerem

Endothelial cells (EC) appear to adapt their morphology and function to the in vivo hemodynamic environment in which they reside. In vitro experiments indicate that similar alterations occur for cultured EC exposed to a laminar steady-state flow-induced shear stress. However, in vivo EC are exposed to a pulsatile flow environment; thus, in this investigation, the influence of pulsatile flow on cell shape and orientation and on actin microfilament localization in confluent bovine aortic endothelial cell (BAEC) monolayers was studied using a 1-Hz nonreversing sinusoidal shear stress of 40 ± 20 dynes/cm2 (type I), 1-Hz reversing sinusoidal shear stresses of 20 ± 40 and 10 ± 15 dynes/cm2 (type II), and 1-Hz oscillatory shear stresses of 0 ± 20 and 0 ± 40 dynes/cm2 (type III). The results show that in a type I nonreversing flow, cell shape changed less rapidly, but cells took on a more elongated shape than their steady flow controls long-term. For low-amplitude type II reversing flow, BAECs changed less rapidly in shape and were always less elongated than their steady controls; however, for high amplitude reversal, BAECs did not stay attached for more than 24 hours. For type III oscillatory flows, BAEC cell shape remained polygonal as in static culture and did not exhibit actin stress fibers, such as occurred in all other flows. These results demonstrate that EC can discriminate between different types of pulsatile flow environments. Furthermore, these experiments indicate the importance of engineering the cell culture environment so as to include pulsatile flow in investigations of vascular endothelial cell biology, whether these studies are designed to study vascular biology and the role of the endothelial cell in disease processes, or are ones leading to the development of hybrid, endothelial cell-preseeded vascular grafts.


2020 ◽  
Vol 236 (1) ◽  
pp. 318-327
Author(s):  
Xiangshan Xu ◽  
Yang Yang ◽  
Guofeng Wang ◽  
Yu Yin ◽  
Shuo Han ◽  
...  

2020 ◽  
Author(s):  
Lei Zhang ◽  
Yuan Li ◽  
Xin Ma ◽  
Xiaojie Wang ◽  
Lingxiao Zhang ◽  
...  

Abstract Background The Fufang Danshen formula is widely used in traditional Chinese medicine for the clinical treatment of coronary heart disease. However, there is no literature reporting the anti-atherosclerotic effect and mechanism of its combination of active ingredients, namely Ginsenoside Rg1-Notoginsenoside R1-Protocatechuic aldehyde (PPR). The aim of this study was to investigate the anti-atherosclerotic effects in ApoE−/− mice and potential mechanism of PPR in low shear stress-injured vascular endothelial cell. Methods In vivo assay, ApoE−/−mice were randomly divided into three groups: model group, Rosuvastatin group, and PPR group, with C57BL/6J mice as control group. A variety of staining methods were utilized for the observation of aortic plaque. The changes of the blood lipid indexes were observed by an automatic biochemistry analyzer. ET-1, eNOS, TAX2, and PGI2 were analyzed by enzymelinked immunosorbent assay. In vitro, we used fluid shear system to induce cell injury and silenced Piezo1 expression in HUVECs by siRNA. We observed the morphological, proliferation, migration and tube formation activity changes of cells after PPR intervention. Quantitative Real-Time PCR and western blot analysis was applied to observe m RNA and protein expression. Results Results showed that PPR treatment reduced atherosclerotic area and lipid level and improved endothelial function in ApoE−/− mice. PPR significantly repaired cell morphology, reduced cell excessive proliferation and ameliorated migration and tube formation activity. In addition, we found that PPR could affect FAK-PI3K/Akt signaling pathways. Importantly, Piezo1 siRNA abolished the protection effects of PPR. Conclusions In summary, our results suggested that PPR ameliorated atherosclerotic plaque formation and endothelial cell injury by intervening the FAK-PI3K/Akt signaling pathways. Piezo1 is a possible target of PPR in the treatment of atherosclerosis. These results indicate that PPR may be apotential drug for atherosclerosis.


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