ArticlePloS one2013
Myeloperoxidase-derived oxidants induce blood-brain barrier dysfunction in vitro and in vivo.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 94 citations in OpenAlex.
- Impact of Neutrophil Extracellular Traps on Clinical Outcome after Subarachnoid Hemorrhage: A Translational Narrative Review.Translational stroke research · 2026Review
- Myeloperoxidase (MPO) Enzymatic Activity, but Not Its Protein Concentration, Is Associated with the Risk of Type 2 Diabetes in Females, Regardless of Obesity Status.Antioxidants (Basel, Switzerland) · 2026Article
- Analyzing the association between MPO levels and glaucoma severity.Biomarkers in medicine · 2025Article
- Repetitive Low-Level Blast Exposure Alters Circulating Myeloperoxidase, Matrix Metalloproteinases, and Neurovascular Endothelial Molecules in Experienced Military Breachers.International journal of molecular sciences · 2025Article
- Lithium reduces cerebral ischemia/reperfusion injury in dexamethasone-treated rats: The role of the PI3K/Akt pathway.Open veterinary journal · 2025Article
- The role of oxidative stress in blood-brain barrier disruption during ischemic stroke: Antioxidants in clinical trials.Biochemical pharmacology · 2024Review
- The Influence of Oxidative Stress Markers in Patients with Ischemic Stroke.Biomolecules · 2024Review
- Benserazide is neuroprotective and improves functional recovery after experimental ischemic stroke by altering the immune response.Scientific reports · 2024Article
- Neuroinflammation in Alzheimer's disease: insights from peripheral immune cells.Immunity & ageing : I & A · 2024Review
- The Role of Neutrophils in Multiple Sclerosis and Ischemic Stroke.Brain sciences · 2024Review
- Hypochlorous acid derived from microglial myeloperoxidase could mediate high-mobility group box 1 release from neurons to amplify brain damage in cerebral ischemia-reperfusion injury.Journal of neuroinflammation · 2024Article
- Lipid biology of plasmalogen-derived halolipids: Signature molecules of myeloperoxidase and eosinophil peroxidase activity.Redox biochemistry and chemistry · 2023Article
- Myeloperoxidase-derived hypochlorous acid targets human airway epithelial plasmalogens liberating protein modifying electrophilic 2-chlorofatty aldehydes.Redox biology · 2023Article
- Neutrophil Heterogeneity and its Roles in the Inflammatory Network after Ischemic Stroke.Current neuropharmacology · 2023Article
- Neutrophils: a subgroup of neglected immune cells in ALS.Frontiers in immunology · 2023Review
- Protocadherin gamma C3: a new player in regulating vascular barrier function.Neural regeneration research · 2023Review
- Chronic Methylmercury Intoxication Induces Systemic Inflammation, Behavioral, and Hippocampal Amino Acid Changes in C57BL6J Adult Mice.International journal of molecular sciences · 2022Article
- Non-Canonical Functions of Myeloperoxidase in Immune Regulation, Tissue Inflammation and Cancer.International journal of molecular sciences · 2022Review
- Myeloperoxidase: a new target for the treatment of stroke?Neural regeneration research · 2022Review
- Effects of acute and chronic oxidative stress on the blood-brain barrier in 2D and 3D in vitro models.Fluids and barriers of the CNS · 2022Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Peripheral leukocytes can exacerbate brain damage by release of cytotoxic mediators that disrupt blood-brain barrier (BBB) function. One of the oxidants released by activated leukocytes is hypochlorous acid (HOCl) formed via the myeloperoxidase (MPO)-H2O2-Cl(-) system. In the present study we examined the role of leukocyte activation, leukocyte-derived MPO and MPO-generated oxidants on BBB function in vitro and in vivo. In a mouse model of lipopolysaccharide (LPS)-induced systemic inflammation, neutrophils that had become adherent released MPO into the cerebrovasculature. In vivo, LPS-induced BBB dysfunction was significantly lower in MPO-deficient mice as compared to wild-type littermates. Both, fMLP-activated leukocytes and the MPO-H2O2-Cl(-) system inflicted barrier dysfunction of primary brain microvascular endothelial cells (BMVEC) that was partially rescued with the MPO inhibitor 4-aminobenzoic acid hydrazide. BMVEC treatment with the MPO-H2O2-Cl(-) system or activated neutrophils resulted in the formation of plasmalogen-derived chlorinated fatty aldehydes. 2-chlorohexadecanal (2-ClHDA) severely compromised BMVEC barrier function and induced morphological alterations in tight and adherens junctions. In situ perfusion of rat brain with 2-ClHDA increased BBB permeability in vivo. 2-ClHDA potently activated the MAPK cascade at physiological concentrations. An ERK1/2 and JNK antagonist (PD098059 and SP600125, respectively) protected against 2-ClHDA-induced barrier dysfunction in vitro. The current data provide evidence that interference with the MPO pathway could protect against BBB dysfunction under (neuro)inflammatory conditions.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.