Low shear stress induced vascular endothelial cell pyroptosis by TET2/SDHB/ROS pathway

2020 ◽  
Author(s):  
Jinna Chen ◽  
Jianwu Zhang ◽  
Jiaxiong Wu ◽  
Shulei Zhang ◽  
Yamin Liang ◽  
...  
Keyword(s):  
Shear Stress ◽  
Endothelial Cell ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Low Shear Stress ◽  
Low Shear

Low shear stress regulates vascular endothelial cell pyroptosis through miR‐181b‐5p/STAT‐3 axis

2020 ◽  
Vol 236 (1) ◽  
pp. 318-327
Author(s):  
Xiangshan Xu ◽  
Yang Yang ◽  
Guofeng Wang ◽  
Yu Yin ◽  
Shuo Han ◽  
...  
Keyword(s):  
Shear Stress ◽  
Endothelial Cell ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Low Shear Stress ◽  
Low Shear

scholarly journals Ginsenoside Rg1-Notoginsenoside R1-Protocatechuic aldehyde attenuates low shear stress-induced vascular endothelial cell dysfunction

2020 ◽  
Author(s):  
Lei Zhang ◽  
Yuan Li ◽  
Xin Ma ◽  
Xiaojie Wang ◽  
Lingxiao Zhang ◽  
...  
Keyword(s):  
Shear Stress ◽  
Endothelial Cell ◽  
Cell Injury ◽  
Vascular Endothelial Cell ◽  
Akt Signaling ◽  
Tube Formation ◽  
Vascular Endothelial ◽  
Ginsenoside Rg1 ◽  
Low Shear Stress ◽  
Low Shear

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.

scholarly journals Ginsenoside Rg1-Notoginsenoside R1-Protocatechuic Aldehyde Reduces Atherosclerosis and Attenuates Low-Shear Stress-Induced Vascular Endothelial Cell Dysfunction

2021 ◽  
Vol 11 ◽  
Author(s):  
Lei Zhang ◽  
Yuan Li ◽  
Xin Ma ◽  
Jiali Liu ◽  
Xiaojie Wang ◽  
...  
Keyword(s):  
Shear Stress ◽  
Endothelial Cell ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Tube Formation ◽  
Vascular Endothelial ◽  
Ginsenoside Rg1 ◽  
Akt Signaling Pathway ◽  
Low Shear Stress ◽  
Low Shear

Background: The Fufang Danshen formula is a clinically important anti-atherosclerotic preparation in traditional Chinese medicine. However, its anti-atherosclerotic effect is not well recognized, and the mechanisms of its combined active ingredients, namely Ginsenoside Rg1-Notoginsenoside R1-Protocatechuic aldehyde (RRP), remain unclear. The purpose of this study was to investigate the anti-atherosclerotic effects and potential mechanism of RRP in ApoE−/− mice and in low-shear stress-injured vascular endothelial cells.Methods: ApoE−/− mice were randomly divided into three groups: model group, rosuvastatin group, and RRP group, with C57BL/6J mice as the control group. Oil-red O, hematoxylin and eosin, Masson, and Movat staining were utilized for the observation of aortic plaque. Changes in the blood lipid indexes were observed with an automatic biochemistry analyzer. ET-1, eNOS, TXA2, and PGI2 levels were analyzed by enzyme-linked immunosorbent assay. In vitro, a fluid shear stress system was used to induce cell injury. Piezo1 expression in HUVECs was silenced using siRNA. Changes in morphology, proliferation, migration, and tube formation activity of cells were observed after RRP treatment. Quantitative Real-Time PCR and western blot analysis were employed to monitor mRNA and protein expression.Results: RRP treatment reduced the atherosclerotic area and lipid levels and improved endothelial function in ApoE−/− mice. RRP significantly repaired cell morphology, reduced excessive cell proliferation, and ameliorated migration and tube formation activity. In addition, RRP affected the FAK-PI3K/Akt signaling pathway. Importantly, Piezo1 silencing abolished the protective effects of RRP.Conclusion: RRP has anti-atherosclerotic effects and antagonizes endothelial cell damage via modulating the FAK-PI3K/Akt signaling pathway. Piezo1 is a possible target of RRP in the treatment of atherosclerosis. Thus, RRP has promising therapeutic potential and broad application prospect for atherosclerosis.

scholarly journals Turbulent fluid shear stress induces vascular endothelial cell turnover in vitro.

1986 ◽  
Vol 83 (7) ◽  
pp. 2114-2117 ◽  
Author(s):  
P. F. Davies ◽  
A. Remuzzi ◽  
E. J. Gordon ◽  
C. F. Dewey ◽  
M. A. Gimbrone
Keyword(s):  
Shear Stress ◽  
Endothelial Cell ◽  
Fluid Shear Stress ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Cell Turnover ◽  
Fluid Shear ◽  
Turbulent Fluid

scholarly journals Low Shear Stress Upregulates CX3CR1 Expression by Inducing VCAM-1 via the NF-κB Pathway in Vascular Endothelial Cells

2020 ◽  
Vol 78 (3) ◽  
pp. 383-389 ◽  
Author(s):  
Yiwei Zhao ◽  
Peile Ren ◽  
Qiufang Li ◽  
Shafiu Adam Umar ◽  
Tan Yang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Protein Expression ◽  
Vascular Endothelial Cells ◽  
Critical Role ◽  
Mrna Levels ◽  
Vascular Endothelial ◽  
Low Shear Stress ◽  
Low Shear ◽  
Cx3cr1 Expression

Abstract Atherosclerosis is a significant cause of mortality and morbidity. Studies suggest that the chemokine receptor CX3CR1 plays a critical role in atherogenesis. Shear stress is an important mechanical force that affects blood vessel function. In this study, we investigated the effect of shear stress on CX3CR1 expression in vascular endothelial cells (VECs). First, cells were exposed to different shear stress and then CX3CR1 mRNA and protein were measured by quantitative RT-PCR and western blot analysis, respectively. CX3CR1 gene silencing was used to analyze the molecular mechanisms underlying shear stress-mediated effects on CX3CR1 expression. CX3CR1 mRNA and protein expression were significantly increased with 4.14 dyne/cm2 of shear stress compared with other tested levels of shear stress. We observed a significant increase in CX3CR1 mRNA levels at 2 h and CX3CR1 protein expression at 4 h. CX3CR1-induced VCAM-1 expression in response to low shear stress by activating NF-κB signaling pathway in VECs. Our findings demonstrate that low shear stress increases CX3CR1 expression, which increases VCAM-1 expression due to elevated NF-κB activation. The current study provides evidence of the correlation between shear stress and atherosclerosis mediated by CX3CR1.

scholarly journals Rac1 mediates laminar shear stress-induced vascular endothelial cell migration

2013 ◽  
Vol 7 (6) ◽  
pp. 472-478 ◽  
Author(s):  
Xianliang Huang ◽  
Yang Shen ◽  
Yi Zhang ◽  
Lin Wei ◽  
Yi Lai ◽  
...  
Keyword(s):  
Shear Stress ◽  
Cell Migration ◽  
Endothelial Cell ◽  
Vascular Endothelial Cell ◽  
Endothelial Cell Migration ◽  
Vascular Endothelial ◽  
Laminar Shear Stress ◽  
Laminar Shear
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