Evidence map›Paper›PMID 25651941›Full record

ArticleBritish journal of pharmacology2015

Endocannabinoids modulate human blood-brain barrier permeability in vitro.

William H Hind, Cristina Tufarelli, Maria Neophytou, Susan I Anderson, Timothy J England, Saoirse E O'Sullivan

Open access · hybridAbstract read
In one paragraph

Article in British journal of pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
9.6field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 96 citations in OpenAlex.

  1. Pooled it
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  3. Astrocyte CBJournal of neuroinflammation · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

William H HindSchool of Medicine, University of Nottingham, Royal Derby Hospital, Derby, UK.
Cristina TufarelliSchool of Medicine, University of Nottingham, Royal Derby Hospital, Derby, UK.
Maria NeophytouSchool of Medicine, University of Nottingham, Royal Derby Hospital, Derby, UK.
Susan I AndersonSchool of Medicine, University of Nottingham, Royal Derby Hospital, Derby, UK.
Timothy J EnglandSchool of Medicine, University of Nottingham, Royal Derby Hospital, Derby, UK.
Saoirse E O'SullivanSchool of Medicine, University of Nottingham, Royal Derby Hospital, Derby, UK.
Royal Derby Hospital · GBUniversity of Nottingham · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeEndocannabinoids alter permeability at various epithelial barriers, and cannabinoid receptors and endocannabinoid levels are elevated by stroke, with potential neuroprotective effects. We therefore explored the role of endocannabinoids in modulating blood-brain barrier (BBB) permeability in normal conditions and in an ischaemia/reperfusion model. EXPERIMENTAL APPROACH: Human brain microvascular endothelial cell and astrocyte co-cultures modelled the BBB. Ischaemia was modelled by oxygen-glucose deprivation (OGD) and permeability was measured by transepithelial electrical resistance. Endocannabinoids or endocannabinoid-like compounds were assessed for their ability to modulate baseline permeability or OGD-induced hyperpermeability. Target sites of action were investigated using receptor antagonists and subsequently identified with real-time PCR. KEY

resultsAnandamide (10 μM) and oleoylethanolamide (OEA, 10 μM) decreased BBB permeability (i.e. increased resistance). This was mediated by cannabinoid CB2 receptors, transient receptor potential vanilloid 1 (TRPV1) channels, calcitonin gene-regulated peptide (CGRP) receptor (anandamide only) and PPARα (OEA only). Application of OEA, palmitoylethanolamide (both PPARα mediated) or virodhamine (all 10 μM) decreased the OGD-induced increase in permeability during reperfusion. 2-Arachidonoyl glycerol, noladin ether and oleamide did not affect BBB permeability in normal or OGD conditions. N-arachidonoyl-dopamine increased permeability through a cytotoxic mechanism. PPARα and γ, CB1 receptors, TRPV1 channels and CGRP receptors were expressed in both cell types, but mRNA for CB2 receptors was only present in astrocytes. CONCLUSION AND IMPLICATION: The endocannabinoids may play an important modulatory role in normal BBB physiology, and also afford protection to the BBB during ischaemic stroke, through a number of target sites.

Indexed as

Arachidonic AcidsAstrocytesBlood-Brain BarrierCells, CulturedCoculture TechniquesElectric ImpedanceEndocannabinoidsEndothelial CellsHumansOleic AcidsPermeabilityPolyunsaturated AlkamidesReceptor, Cannabinoid, CB2Reperfusion InjuryRNA, MessengeranandamideArachidonic AcidsEndocannabinoidsOleic AcidsoleoylethanolamidePolyunsaturated AlkamidesReceptor, Cannabinoid, CB2RNA, Messenger

Identifiers

PMID25651941
PMCPMC4459020
OpenAlexW1578641739

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.