ArticleAmerican journal of physiology. Heart and circulatory physiology2013
H2O2-induced endothelial NO production contributes to vascular cell apoptosis and increased permeability in rat venules.
Article in American journal of physiology. Heart and circulatory physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Reduced flow-and acetylcholine-induced dilations in visceral compared to subcutaneous adipose arterioles in human morbid obesity.Microcirculation (New York, N.Y. : 1994) · 2015Trial
- Quercetin Protects Blood-Brain Barrier Integrity and Maintains Microvascular Permeability Following Traumatic Brain Injury.Neurocritical care · 2025Article
- Leveraging avidin-biotin interaction to quantify permeability property of microvessels-on-a-chip networks.American journal of physiology. Heart and circulatory physiology · 2022Article
- Dietary Supplementation withAnimals : an open access journal from MDPI · 2021Article
- The mitochondrial thioredoxin reductase system (TrxR2) in vascular endothelium controls peroxynitrite levels and tissue integrity.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Heme Oxygenase-1 at the Nexus of Endothelial Cell Fate Decision Under Oxidative Stress.Frontiers in cell and developmental biology · 2021Article
- Oxidative Stress and Microvessel Barrier Dysfunction.Frontiers in physiology · 2020Review
- HPhysiological reports · 2019Article
- Cytoprotective role of vitamin E in porcine adipose-tissue-derived mesenchymal stem cells against hydrogen-peroxide-induced oxidative stress.Cell and tissue research · 2018Article
- New insights into shear stress-induced endothelial signalling and barrier function: cell-free fluid versus blood flow.Cardiovascular research · 2017Article
- Development and Characterization of In Vitro Microvessel Network and Quantitative Measurements of Endothelial [Ca2+]i and Nitric Oxide Production.Journal of visualized experiments : JoVE · 2016Article
- Wall stretch and thromboxane A₂ activate NO synthase (eNOS) in pulmonary arterial smooth muscle cells via H₂O₂ and Akt-dependent phosphorylation.Pflugers Archiv : European journal of physiology · 2016Article
- In vitro recapitulation of functional microvessels for the study of endothelial shear response, nitric oxide and [Ca2+]i.PloS one · 2015Article
- Acute exertion elicits a H2O2-dependent vasodilator mechanism in the microvasculature of exercise-trained but not sedentary adults.Hypertension (Dallas, Tex. : 1979) · 2015Article
- A1 adenosine receptor negatively modulates coronary reactive hyperemia via counteracting A2A-mediated H2O2 production and KATP opening in isolated mouse hearts.American journal of physiology. Heart and circulatory physiology · 2013Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Although elevated levels of H(2)O(2) have been implicated to play important roles in the pathogenesis of various cardiovascular diseases, the underlying mechanisms remain unclear. This study aims to examine the effect of H(2)O(2) on endothelial nitric oxide (NO) production in intact venules, and elucidate the role and mechanisms of NO in H(2)O(2)-induced increases in microvessel permeability. Experiments were conducted on individually perfused rat mesenteric venules. Microvessel permeability was determined by measuring hydraulic conductivity (Lp), and endothelial [Ca(2+)](i) was measured on fura-2-loaded vessels. Perfusion of H(2)O(2) (10 μM) caused a delayed and progressively increased endothelial [Ca(2+)](i) and Lp, a pattern different from inflammatory mediator-induced immediate and transient response. Under the same experimental conditions, measuring endothelial NO via DAF-2 and the spatial detection of cell apoptosis by fluorescent markers revealed that H(2)O(2) induced two phases of NO production followed by caspase activation, intracellular Ca(2+) accumulation, and vascular cell apoptosis. The initial NO production was correlated with increased endothelial NO synthase (eNOS) Ser(1177) phosphorylation in the absence of elevated endothelial [Ca(2+)](i), whereas the second phase of NO depended on increased [Ca(2+)](i) and was associated with Thr(495) dephosphorylation without increased Ser(1177) phosphorylation. Inhibition of NOS prevented H(2)O(2)-induced caspase activation, cell apoptosis, and increases in endothelial [Ca(2+)](i) and Lp. Our results indicate that H(2)O(2) at micromolar concentration is able to induce a large magnitude of NO in intact venules, causing caspase activation-mediated endothelial Ca(2+) accumulation, cell apoptosis, and increases in permeability. The mechanisms revealed from intact microvessels may contribute to the pathogenesis of oxidant-related cardiovascular diseases.
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