ArticleNitric oxide : biology and chemistry2019
Regulation of endothelial barrier integrity by redox-dependent nitric oxide signaling: Implication in traumatic and inflammatory brain injuries.
Article in Nitric oxide : biology and chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 18 citations in OpenAlex.
- The GPR68-NINJ1 axis: an emerging mechano-chemical checkpoint in blood-brain barrier disruption-a hypothetical framework and therapeutic promise.Frontiers in cellular neuroscience · 2026Article
- Immunomodulatory and anti-inflammatory potential of S-nitrosoglutathione (GSNO) in multiple sclerosis: a review of mechanisms and therapeutic perspectives.Frontiers in immunology · 2026Review
- Neurogranin-MYH9 interaction regulates cytoskeletal remodeling in cerebral vasculature.Fluids and barriers of the CNS · 2025Article
- Salivary-Gland-Mediated Nitrate Recirculation as a Modulator for Cardiovascular Diseases.Biomolecules · 2025Review
- The role of S-nitrosoglutathione reductase (GSNOR) in T cell-mediated immunopathology of experimental autoimmune encephalomyelitis (EAE).Neuroscience · 2025Article
- REsveratrol for VAscular cognitive impairment investigating cerebral Metabolism and Perfusion (REVAMP trial): a study protocol for a randomized, double-blind, placebo-controlled trial.Frontiers in nutrition · 2024Article
- Angiotensin II-induced endothelial dysfunction: Impact of sex, genetic background, and rho kinase.Physiological reports · 2022Article
- Vascular and immunopathological role of Asymmetric Dimethylarginine (ADMA) in Experimental Autoimmune Encephalomyelitis.Immunology · 2021Article
- Hydroxyethylstarch revisited for acute brain injury treatment.Neural regeneration research · 2021Review
- Molecular Dambusters: What Is Behind Hyperpermeability in Bradykinin-Mediated Angioedema?Clinical reviews in allergy & immunology · 2021Review
- Asymmetric dimethylarginine exacerbates cognitive dysfunction associated with cerebrovascular pathology.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Evaluation of Gas Explosion Injury Based on Analysis of Rat Serum Profile by Ultra-Performance Liquid Chromatography/Mass Spectrometry-Based Metabonomics Techniques.BioMed research international · 2020Article
- Piezo1 acts upstream of TRPV4 to induce pathological changes in endothelial cells due to shear stress.The Journal of biological chemistryArticle
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7 authors at 1 institution in 1 country.
Funding
Abstract
Nitric oxide (NO) synthesized by eNOS plays a key role in regulation of endothelial barrier integrity but underlying cell signaling pathway is not fully understood at present. Here, we report opposing roles of two different redox-dependent NO metabolites; peroxynitrite (ONOO-) vs. S-nitrosoglutathione (GSNO), in cell signaling pathways for endothelial barrier disruption. In cultured human brain microvessel endothelial cells (hBMVECs), thrombin induced F-actin stress fiber formation causes barrier disruption via activating eNOS. Thrombin induced eNOS activity participated in cell signaling (e.g. RhoA and calcium influx mediated phosphorylation of myosin light chain) for F-actin stress fiber formation by increasing ONOO- levels. On the other hand, thrombin had no effect on intracellular levels of S-nitrosoglutathione (GSNO), another cellular NO metabolite. However, exogenous GSNO treatment attenuated the thrombin-induced cell signaling pathways for endothelial barrier disruption, thus suggesting the role of a shift of NO metabolism (GSNO vs. ONOO-) toward ONOO- synthesis in cell signaling for endothelial barrier disruption. Consistent with these in vitro studies, in animal models of traumatic brain injury and experimental autoimmune encephalomyelitis (EAE), ONOO- scavenger treatment as well as GSNO treatment were effective for attenuation of BBB leakage, edema formation, and CNS infiltration of mononuclear cells. Taken together, these data document that eNOS-mediated NO production and following redox-dependent NO metabolites (ONOO- vs. GSNO) are potential therapeutic target for CNS microvascular disease (traumatic and inflammatory) pathologies.
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