ArticleFree radical biology & medicine2010
A novel role for caveolin-1 in regulating endothelial nitric oxide synthase activation in response to H2O2 and shear stress.
Article in Free radical biology & medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 35 citations in OpenAlex.
- S1P (Sphingosine-1-Phosphate)-Induced Vasodilation in Human Resistance Arterioles During Health and Disease.Hypertension (Dallas, Tex. : 1979) · 2022Article
- Sweat the small stuff: The human microvasculature and heart disease.Microcirculation (New York, N.Y. : 1994) · 2021Review
- Caveolae and lipid sorting: Shaping the cellular response to stress.The Journal of cell biology · 2020Review
- Orthostatic Challenge Shifts the Hemostatic System of Patients Recovered from Stroke toward Hypercoagulability.Frontiers in physiology · 2017Article
- Asymmetric Dimethylarginine Stimulates Akt1 Phosphorylation via Heat Shock Protein 70-Facilitated Carboxyl-Terminal Modulator Protein Degradation in Pulmonary Arterial Endothelial Cells.American journal of respiratory cell and molecular biology · 2016Article
- ROS signaling and redox biology in endothelial cells.Cellular and molecular life sciences : CMLS · 2015Review
- Csk-Induced Phosphorylation of Src at Tyrosine 530 is Essential for H2O2-Mediated Suppression of ERK1/2 in Human Umbilical Vein Endothelial Cells.Scientific reports · 2015Article
- Endothelin-1 induces a glycolytic switch in pulmonary arterial endothelial cells via the mitochondrial translocation of endothelial nitric oxide synthase.American journal of respiratory cell and molecular biology · 2014Article
- Endothelin-1 stimulates catalase activity through the PKCδ-mediated phosphorylation of serine 167.Free radical biology & medicine · 2014Article
- Disruption of endothelial cell mitochondrial bioenergetics in lambs with increased pulmonary blood flow.Antioxidants & redox signaling · 2013Article
- Asymmetric dimethylarginine induces endothelial nitric-oxide synthase mitochondrial redistribution through the nitration-mediated activation of Akt1.The Journal of biological chemistry · 2013Article
- Specific visualization of nitric oxide in the vasculature with two-photon microscopy using a copper based fluorescent probe.PloS one · 2013Article
- Apolipoprotein E enhances endothelial-NO production by modulating caveolin 1 interaction with endothelial NO synthase.Hypertension (Dallas, Tex. : 1979) · 2012Article
- Role of reactive oxygen and nitrogen species in the vascular responses to inflammation.Free radical biology & medicine · 2012Review
- eNOS activation and NO function: structural motifs responsible for the posttranslational control of endothelial nitric oxide synthase activity.The Journal of endocrinology · 2011Review
- Placenta growth factor expression is regulated by hydrogen peroxide in vascular smooth muscle cells.American journal of physiology. Cell physiology · 2011Article
- Oxidative stress and the development of endothelial dysfunction in congenital heart disease with increased pulmonary blood flow: lessons from the neonatal lamb.Trends in cardiovascular medicine · 2010Review
- Vascular Nitric Oxide: Formation and Function.Journal of blood medicine · 2010Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Previous studies have shown that acute increases in oxidative stress induced by the addition of hydrogen peroxide (H(2)O(2)) can increase endothelial nitric oxide synthase (eNOS) catalytic activity via an increase in the phosphorylation of eNOS at serine 1177. However, it is unclear how increased H(2)O(2) affects nitric oxide (NO) signaling when endothelial cells are exposed to biomechanical forces. Thus, the purpose of this study was to evaluate the acute effects of H(2)O(2) on NO signaling in the presence or absence of laminar shear stress. We found that acute sustained increases in cellular H(2)O(2) levels in bovine aortic endothelial cells did not alter basal NO generation but the NO produced in response to shear stress was significantly increased. This amplification in NO signaling was found to correlate with an H(2)O(2)-induced increase in eNOS localized to the plasma membrane and an increase in total caveolin-1 protein levels. We further demonstrated that overexpressing caveolin-1 increased eNOS localized to the plasma membrane again without altering total eNOS protein levels. We also found that caveolin-1 overexpression increased NO generation in response to shear stress but only in the presence of H(2)O(2). Conversely, depleting caveolin-1 with an siRNA decreased eNOS localized to the plasma membrane and abolished the enhanced NO generation. Finally, we found that expressing a caveolin-1 binding-site deletion mutant of eNOS in COS-7 cells decreased its plasma membrane localization and resulted in attenuated NO production in response to calcium activation. In conclusion, we have identified a new role for caveolin-1 in enhancing eNOS trafficking to the plasma membrane that seems to be involved in priming eNOS for flow-mediated activation under conditions of oxidative stress. To our knowledge, this is the first report that H(2)O(2) modulates eNOS activity by altering its subcellular location and that caveolin-1 can play a stimulatory role in NO signaling.
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