Evidence map›Paper›PMID 24644287›Full record

ArticleThe Journal of biological chemistry2014

The endocannabinoid/endovanilloid N-arachidonoyl dopamine (NADA) and synthetic cannabinoid WIN55,212-2 abate the inflammatory activation of human endothelial cells.

Kevin Wilhelmsen, Samira Khakpour, Alphonso Tran, Kayla Sheehan, Mark Schumacher, Fengyun Xu, Judith Hellman

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
5.2field-weighted citation impact, top 5% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. The Impact of the CBMolecules (Basel, Switzerland) · 2024
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  11. Review
  12. GPR18-Mediated Relaxation of Human Isolated Pulmonary Arteries.International journal of molecular sciences · 2022
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Cannabinoids, the Heart of the Matter.Journal of the American Heart Association · 2018
    Review
  19. Article
  20. Article
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

7 authors at 1 institution in 1 country.

Kevin WilhelmsenFrom the Department of Anesthesia and Perioperative Care.
Samira Khakpour
Alphonso Tran
Kayla Sheehan
Mark Schumacher
Fengyun Xu
Judith Hellman
University of California, San Francisco · US

Funding

MOLECULAR AND CELLULAR IMMUNOLOGYT32AI007334 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CYSTER, JASON G · 1988 to 2023
$11.0M
NIAID NIH HHS T32 AI007334
6 · The paper itself

Abstract

Although cannabinoids, such as Δ(9)-tetrahydrocannabinol, have been studied extensively for their psychoactive effects, it has become apparent that certain cannabinoids possess immunomodulatory activity. Endothelial cells (ECs) are centrally involved in the pathogenesis of organ injury in acute inflammatory disorders, such as sepsis, because they express cytokines and chemokines, which facilitate the trafficking of leukocytes to organs, and they modulate vascular barrier function. In this study, we find that primary human ECs from multiple organs express the cannabinoid receptors CB1R, GPR18, and GPR55, as well as the ion channel transient receptor potential cation channel vanilloid type 1. In contrast to leukocytes, CB2R is only minimally expressed in some EC populations. Furthermore, we show that ECs express all of the known endocannabinoid (eCB) metabolic enzymes. Examining a panel of cannabinoids, we demonstrate that the synthetic cannabinoid WIN55,212-2 and the eCB N-arachidonoyl dopamine (NADA), but neither anandamide nor 2-arachidonoylglycerol, reduce EC inflammatory responses induced by bacterial lipopeptide, LPS, and TNFα. We find that endothelial CB1R/CB2R are necessary for the effects of NADA, but not those of WIN55,212-2. Furthermore, transient receptor potential cation channel vanilloid type 1 appears to counter the anti-inflammatory properties of WIN55,212-2 and NADA, but conversely, in the absence of these cannabinoids, its inhibition exacerbates the inflammatory response in ECs activated with LPS. These data indicate that the eCB system can modulate inflammatory activation of the endothelium and may have important implications for a variety of acute inflammatory disorders that are characterized by EC activation.

Indexed as

AnalgesicsArachidonic AcidsBacterial ProteinsBenzoxazinesCannabinoidsDopamineHumansHuman Umbilical Vein Endothelial CellsInflammationLipopeptidesMorpholinesNaphthalenesReceptors, CannabinoidTRPV Cation Channels(3R)-((2,3-dihydro-5-methyl-3-((4-morpholinyl)methyl)pyrrolo-(1,2,3-de)-1,4-benzoxazin-6-yl)(1-naphthalenyl))methanoneAnalgesicsArachidonic Acidsarachidonyl dopamineBacterial ProteinsBenzoxazinesCannabinoidsDopamineLipopeptidesMorpholinesNaphthalenesReceptors, CannabinoidTRPV1 receptorTRPV Cation ChannelsCannabinoid ReceptorsCannabinoidsEndocannabinoidsEndothelial CellEndothelial DysfunctionEndotheliumSepsisToll-like Receptors (TLR)TRP Channels

Identifiers

PMID24644287
PMCPMC4036321
OpenAlexW1974363838

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.