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Nitric oxide synthase expression in endothelial cells exposed to mechanical forces
T Ziegler1, P Silacci, V J Harrison
1Division of Hypertension and Vascular Medicine, CHUV, Lausanne, Switzerland.
Hypertension (Dallas, Tex. : 1979)
|August 27, 1998
Summary
Mechanical forces like shear stress regulate endothelial nitric oxide synthase (eNOS) expression. Unidirectional shear stress increases eNOS mRNA transcriptionally, while oscillatory shear and stretch involve post-transcriptional regulation.
Area of Science:
- Vascular Biology
- Molecular Biology
- Cellular Mechanics
Background:
- Nitric oxide (NO) is crucial in vascular biology and pathobiology.
- Endothelial NO synthase (eNOS) expression is influenced by mechanical factors from blood flow.
Purpose of the Study:
- To investigate the correlation between eNOS mRNA expression and promoter activation in endothelial cells under mechanical stress.
- To differentiate the effects of shear stress and cyclic stretch on eNOS regulation.
Main Methods:
- Bovine aortic endothelial cells (BAECs) and human umbilical vein endothelial cells (EA hy.926) were subjected to unidirectional and oscillatory shear stress, and cyclic stretch.
- eNOS mRNA levels were quantified using Northern blot analysis.
- eNOS promoter activity was measured via luciferase reporter assays after transfection.
Main Results:
- Unidirectional shear stress increased eNOS mRNA expression and promoter activity.
- Oscillatory shear had varied effects on eNOS mRNA but significantly activated the promoter.
- Cyclic stretch did not alter eNOS mRNA but reduced promoter activation.
Conclusions:
- Unidirectional shear stress upregulates eNOS mRNA expression through transcriptional mechanisms.
- Oscillatory shear stress and cyclic stretch appear to regulate eNOS expression via post-transcriptional mechanisms.