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Human Saphenous Vein Endothelial Cell Isolation and Exposure to Controlled Levels of Shear Stress and Stretch
Published on: April 21, 2023
Low Shear Stress Upregulates CX3CR1 Expression by Inducing VCAM-1 via the NF-κB Pathway in Vascular Endothelial Cells
Yiwei Zhao1, Peile Ren1, Qiufang Li2
1Department of Physiology, School of Medicine, Xinjiang Medical University, Urumqi, 830011, Xinjiang, PR China.
Insights
Low shear stress significantly increases CX3CR1 expression in vascular endothelial cells, promoting VCAM-1 expression via NF-κB activation. This links mechanical forces to atherosclerosis development through CX3CR1 signaling.
Area of Science:
- Cardiovascular Biology
- Mechanobiology
- Molecular Medicine
Background:
- Atherosclerosis is a major cause of death and disease.
- The chemokine receptor CX3CR1 is implicated in atherogenesis.
- Shear stress is a key mechanical factor influencing vascular health.
Purpose of the Study:
- To investigate the impact of shear stress on CX3CR1 expression in vascular endothelial cells (VECs).
- To elucidate the molecular mechanisms by which shear stress affects CX3CR1 levels.
- To understand the role of CX3CR1 in shear stress-induced VCAM-1 expression.
Main Methods:
- VECs were exposed to varying levels of shear stress.
- CX3CR1 mRNA and protein levels were quantified using RT-PCR and Western blot.
- CX3CR1 gene silencing was employed to study molecular pathways.
- NF-κB activation was assessed to understand signaling.
Main Results:
- A shear stress level of 4.14 dyne/cm² significantly upregulated CX3CR1 mRNA and protein expression.
- CX3CR1 mRNA increased at 2 hours, and protein levels at 4 hours post-shear stress.
- Low shear stress-induced VCAM-1 expression was mediated by CX3CR1 via NF-κB pathway activation.
Conclusions:
- Low shear stress enhances CX3CR1 expression in VECs.
- Increased CX3CR1 expression promotes VCAM-1 upregulation through NF-κB signaling.
- This study establishes a link between shear stress, CX3CR1, and atherosclerosis development.
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.
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