Evidence map›Paper›PMID 25395667›Full record

ArticleBiology open2014

TRPV1 mediates cellular uptake of anandamide and thus promotes endothelial cell proliferation and network-formation.

Nicole A Hofmann, Sonja Barth, Markus Waldeck-Weiermair, Christiane Klec, Dirk Strunk, Roland Malli, Wolfgang F Graier

Abstract read
In one paragraph

Article in Biology open, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
–field-weighted citation impact
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

24 citing papers in PubMed.

  1. Journal of Zhejiang University. Science. B · 2026
    Review
  2. Review
  3. Review
  4. Article
  5. Transient Receptor Potential (TRP) Channels in Tumor Vascularization.International journal of molecular sciences · 2022
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Suppression of Presynaptic Glutamate Release by Postsynaptic Metabotropic NMDA Receptor Signalling to Pannexin-1.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Review
  20. Endothelial CaInternational journal of molecular sciences · 2018
    Review
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.

Nicole A HofmannInstitute for Molecular Biology and Biochemistry, Medical University of Graz, A-8010 Graz, Austria.
Sonja BarthInstitute for Molecular Biology and Biochemistry, Medical University of Graz, A-8010 Graz, Austria.
Markus Waldeck-WeiermairInstitute for Molecular Biology and Biochemistry, Medical University of Graz, A-8010 Graz, Austria.
Christiane KlecInstitute for Molecular Biology and Biochemistry, Medical University of Graz, A-8010 Graz, Austria.
Dirk StrunkExperimental and Clinical Cell Therapy Institute, Paracelsus Medical University, A-5020 Salzburg, Austria.
Roland MalliInstitute for Molecular Biology and Biochemistry, Medical University of Graz, A-8010 Graz, Austria.
Wolfgang F GraierInstitute for Molecular Biology and Biochemistry, Medical University of Graz, A-8010 Graz, Austria wolfgang.graier@medunigraz.at.

Funding

Austrian Science Fund FWF P 20181Austrian Science Fund FWF P 21857Austrian Science Fund FWF P 22553Austrian Science Fund FWF W 1226
6 · The paper itself

Abstract

Anandamide (N-arachidonyl ethanolamide, AEA) is an endogenous cannabinoid that is involved in various pathological conditions, including cardiovascular diseases and tumor-angiogenesis. Herein, we tested the involvement of classical cannabinoid receptors (CBRs) and the Ca(2+)-channel transient receptor potential vanilloid 1 (TRPV1) on cellular AEA uptake and its effect on endothelial cell proliferation and network-formation. Uptake of the fluorescence-labeled anandamide (SKM4-45-1) was monitored in human endothelial colony-forming cells (ECFCs) and a human endothelial-vein cell line (EA.hy926). Involvement of the receptors during AEA translocation was determined by selective pharmacological inhibition (AM251, SR144528, CID16020046, SB366791) and molecular interference by TRPV1-selective siRNA-mediated knock-down and TRPV1 overexpression. We show that exclusively TRPV1 contributes essentially to AEA transport into endothelial cells in a Ca(2+)-independent manner. This TRPV1 function is a prerequisite for AEA-induced endothelial cell proliferation and network-formation. Our findings point to a so far unknown moonlighting function of TRPV1 as Ca(2+)-independent contributor/regulator of AEA uptake. We propose TRPV1 as representing a promising target for development of pharmacological therapies against AEA-triggered endothelial cell functions, including their stimulatory effect on tumor-angiogenesis.

Indexed as

anandamide, AEAanandamide transportangiogenesisendothelial colony-forming cells, ECFCnetwork-formationproliferationtransient receptor potential vanilloid 1, TRPV1

Identifiers

PMID25395667
PMCPMC4265754

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Registered trials

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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.