Shear stress induction of the endothelial nitric oxide synthase gene is calcium‐dependent but not calcium‐activated

Xiao, Zeshuai; Zhang, Zhaohui; Diamond, Scott L.

doi:10.1002/(sici)1097-4652(199705)171:2<205::aid-jcp11>3.3.co;2-3

Cited by 26 publications

(31 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…8 In this model, ECs located in the region of DLF exhibited polygonal morphology, and further downstream in the region of ULF, they were elongated. Consistent with previous reports, 11,71,72 eNOS expression was significantly increased in response to ULF compared with static conditions. In the DLF region, eNOS expression was also increased relative to static controls, but the increase was small relative to the ULF region and was not statistically significant.…”

Section: Discussionsupporting

confidence: 92%

Relative Reduction of Endothelial Nitric-Oxide Synthase Expression and Transcription in Atherosclerosis-Prone Regions of the Mouse Aorta and in an in Vitro Model of Disturbed Flow

Won

Zhu

Chen

et al. 2007

The American Journal of Pathology

118

View full text Add to dashboard Cite

Atherosclerosis develops in distinct regions of the arterial tree. Defining patterns and mechanisms of endothelial cell gene expression in different regions of normal arteries is key to understanding the initial molecular events in atherogenesis. In this study, we demonstrated that the expression of endothelial nitric-oxide synthase (eNOS), an atheroprotective gene, and its phosphorylation on Ser 1177 , a marker of activity, were lower in regions of the normal mouse aorta that are predisposed to atherosclerosis. The same expression pattern was observed in mouse strains that are both susceptible and resistant to atherosclerosis, and the topography of eNOS expression was inverse to p65, the main nuclear factor-B subunit. Modeling of disturbed and uniform laminar flow in vitro reproduced the expression patterns of eNOS and p65 that were found in vivo. Heterogeneous nuclear RNA expression and RNA polymerase II chromosome immunoprecipitation studies demonstrated that regulation of transcription contributed to increased eNOS expression in response to shear stress. In vivo, the transcription of eNOS was reduced in regions of the mouse aorta predisposed to atherosclerosis, as defined by reporter gene expression in eNOS promoter-␤-galactosidase reporter transgenic mice. These data suggest that disturbed hemodynamic patterns found at arterial branches and curvatures uniquely modulate endothelial cell gene expression by regulating transcription , potentially explaining why these regions preferentially develop atherosclerosis when risk factors such as hypercholesterolemia are introduced.

show abstract

Section: Discussionsupporting

confidence: 92%

Relative Reduction of Endothelial Nitric-Oxide Synthase Expression and Transcription in Atherosclerosis-Prone Regions of the Mouse Aorta and in an in Vitro Model of Disturbed Flow

Won

Zhu

Chen

et al. 2007

The American Journal of Pathology

118

View full text Add to dashboard Cite

show abstract

“…The most profound of these changes is the increase in NO release with increasing shear stress. Shear stress causes rapid eNOS activation and upregulates eNOS gene expression by transcription activation of the eNOS promoter (Xiao et al, 1997).…”

Section: Endothelial Cell Responses To Shear Stressmentioning

confidence: 99%

Endothelial cell functions

Michiels

2003

Journal Cellular Physiology

622

429

View full text Add to dashboard Cite

Endothelial cells play a wide variety of critical roles in the control of vascular function. Indeed, since the early 1980s, the accumulating knowledge of the endothelial cell structure as well as of the functional properties of the endothelial cells shifted their role from a passive membrane or barrier to a complex tissue with complex functions adaptable to needs specific in time and location. Hence, it participates to all aspects of the vascular homeostasis but also to physiological or pathological processes like thrombosis, inflammation, or vascular wall remodeling. Some of the most important endothelial functions will be described in the following review and more specifically, their role in blood vessel formation, in coagulation and fibribolysis, in the regulation of vascular tone as well as their participation in inflammatory reactions and in tumor neoangiogenesis. J. Cell. Physiol. 196: 430–443, 2003. © 2003 Wiley‐Liss, Inc.

show abstract

“…However, vibration-induced stress and strain on peripheral vessels could also have a direct effect on vascular function by altering NO concentrations. For example, previous studies have demonstrated that flow-induced shear stress on endothelial cells stimulates NOS-3 levels and NOS-3-mediated NO production [29][30][31] . In this study, the shear stress induced by vibration resulted in an increase in NOS-2 and NOS-3 expression in arteries of obese, but not vibrated rats.…”

Section: Fig 6 Dose-dependent Vasodilation To the No Donor Snap Inmentioning

confidence: 99%

Vibration Disrupts Vascular Function in a Model of Metabolic Syndrome

et al. 2009

View full text Add to dashboard Cite

Shear stress induction of the endothelial nitric oxide synthase gene is calcium‐dependent but not calcium‐activated

Cited by 26 publications

References 0 publications

Relative Reduction of Endothelial Nitric-Oxide Synthase Expression and Transcription in Atherosclerosis-Prone Regions of the Mouse Aorta and in an in Vitro Model of Disturbed Flow

Relative Reduction of Endothelial Nitric-Oxide Synthase Expression and Transcription in Atherosclerosis-Prone Regions of the Mouse Aorta and in an in Vitro Model of Disturbed Flow

Endothelial cell functions

Vibration Disrupts Vascular Function in a Model of Metabolic Syndrome

Contact Info

Product

Resources

About