Exogenous arachidonic acid mediates permeability of human brain microvessel endothelial cells through prostaglandin E 2 activation of EP 3 and EP 4 receptors
Open accessAbstract
The blood–brain barrier, formed by microvessel endothelial cells, is the restrictive barrier between the brain parenchyma and the circulating blood. Arachidonic acid ( ARA ; 5,8,11,14‐ cis ‐eicosatetraenoic acid) is a conditionally essential polyunsaturated fatty acid [20:4( n − 6)] and is a major constituent of brain lipids. The current study examined the transport processes for ARA in confluent monolayers of human brain microvascular endothelial cells ( HBMEC ). Addition of radioactive ARA to the apical compartment of HBMEC cultured on Transwell ® inserts resulted in rapid incorporation of radioactivity into the basolateral medium. Knock down of fatty acid transport proteins did not alter ARA passage into the basolateral medium as a result of the rapid generation of prostaglandin E 2 ( PGE 2 ), an eicosanoid known to facilitate opening of the blood–brain barrier. Permeability following ARA or PGE 2 exposure was confirmed by an increased movement of fluorescein‐labeled dextran from apical to basolateral medium. ARA ‐mediated permeability was attenuated by specific cyclooxygenase‐2 inhibitors. EP 3 and EP 4 receptor antagonists attenuated the ARA ‐mediated permeability of HBMEC . The results indicate that ARA increases permeability of HBMEC monolayers likely via increased production of PGE 2 which acts upon EP 3 and EP 4 receptors to mediate permeability. These observations may explain the rapid influx of ARA into the brain previously observed upon plasma infusion with ARA . image The blood–brain barrier, formed by microvessel endothelial cells, is a restrictive barrier between the brain parenchyma and the circulating blood. Radiolabeled arachidonic acid (ARA) movement across, and monolayer permeability in the presence of ARA, was examined in confluent monolayers of primary human brain microvessel endothelial cells (HBMECs) cultured on Transwell ® plates. Incubation of HBMECs with ARA resulted in a rapid increase in HBMEC monolayer permeability. The mechanism was mediated, in part, through increased prostaglandin E 2 production from ARA which acted upon EP 3 and EP 4 receptors to increase HBMEC monolayer permeability.
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Stimulation of endothelial cells with Aβ or proinflammatory cytokines reduced expression of tight junction proteins Claudin-5, VE-cadherin and Occludin, thus increasing permeability.
“Multiple in vitro experiments revealed that stimulation of endothelial cells with Aβ or proinflammatory cytokines reduced the expression of tight junction proteins like Claudin-5, VE-cadherin and Occludin, thus increased permeability.474–478”
From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [477]
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- Authors
- Dalvi, S., Nguyen, H. H., On, N., Mitchell, R. W., Aukema, H. M., Miller, D. W., & Hatch, G. M.
- Affiliations
- Children's Hospital Research Institute of Manitoba (CA)
- Corresponding author
- Hatch, Grant M.
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2015-04-27
- Volume
- 135
- Issue
- 5
- Pages
- 867-879
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- OpenAlex
- W2102125353
- Cited by
- 37
- References
- 56
- Citations by year
- 2026: 5 · 2025: 5 · 2024: 3 · 2023: 3 · 2022: 4 · 2021: 4 · 2020: 1 · 2019: 2 · 2018: 3 · 2017: 1 · 2016: 1 · 2015: 5
- FWCI
- 1.78
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neurochemistry (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Canadian Institutes of Health Research
- Heart and Stroke Foundation of Canada
- Natural Sciences and Engineering Research Council of Canada
- Manitoba Health Research Council
- Topics
- Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
- Health Sciences › Medicine › Pharmacology › Inflammatory mediators and NSAID effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Eicosanoids and Hypertension Pharmacology
- Keywords
- arachidonic acid, blood-brain barrier, brain microvascular endothelial cells, endothelial permeability, prostaglandin E2, EP3 receptor, EP4 receptor, cyclooxygenase-2, fatty acid uptake, eicosanoids
- MeSH terms
- Brain, Capillary Permeability, Cells, Cultured, Dextrans, Gene Expression Regulation, Humans, Isotopes, Prostaglandin Antagonists, Dinoprostone, Arachidonic Acid, CD36 Antigens, Oleic Acid, Organic Anion Transporters, RNA, Small Interfering, Endothelial Cells, Cyclooxygenase 1, Cyclooxygenase 2, Microvessels, Receptors, Prostaglandin E, EP3 Subtype, Receptors, Prostaglandin E, EP4 Subtype
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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