Evidence map›Paper›PMID 24249637›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2014

Lysophosphatidic acid induces vasodilation mediated by LPA1 receptors, phospholipase C, and endothelial nitric oxide synthase.

Éva Ruisanchez, Péter Dancs, Margit Kerék, Tamás Németh, Bernadett Faragó, Andrea Balogh, Renukadevi Patil, Brett L Jennings, Károly Liliom, Kafait U Malik and 3 more

Open access · greenAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 23% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Association between endothelial nitric oxide synthase 894G>T polymorphism and prostate cancer risk: a meta-analysis of literature studies.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Pooled it
  2. Article
  3. Article
  4. Role of G-protein coupled receptors in cardiovascular diseases.Frontiers in cardiovascular medicine · 2023
    Review
  5. Article
  6. Article
  7. Article
  8. Lysophosphatidic acid acts on LPABritish journal of pharmacology · 2018
    Article
  9. Autotaxin⁻Lysophosphatidic Acid Signaling in Alzheimer's Disease.International journal of molecular sciences · 2018
    Review
  10. LPAFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017
    Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. 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

13 authors at 4 institutions in 2 countries.

Éva Ruisanchez1Z.B., Institute of Human Physiology and Clinical Experimental Research, Semmelweis University, POB 448, H-1446 Budapest, Hungary. benyo.zoltan@med.semmelweis-univ.hu.
Péter Dancs
Margit Kerék
Tamás Németh
Bernadett Faragó
Andrea Balogh
Renukadevi Patil
Brett L Jennings
Károly Liliom
Kafait U Malik
Alan V Smrcka
Gabor Tigyi
Zoltán Benyó
Semmelweis University · HUUniversity of Tennessee Health Science Center · USHUN-REN Research Centre for Natural Sciences · HUUniversity of Rochester · US

Funding

Ligand Recognition by Phospholipid Growth Factor ReceptorsR01CA092160 · NCI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI TIGYI, GABOR J · 2001 to 2022
$5.9M
SIGNAL TRANSDUCTION BY G PROTEINR01GM053536 · NIGMS · UNIVERSITY OF ROCHESTER · PI SMRCKA, ALAN V. · 1996 to 2018
$4.9M
NCI NIH HHS R01 CA092160NIGMS NIH HHS R01 GM053536
6 · The paper itself

Abstract

Lysophosphatidic acid (LPA) has been implicated as a mediator of several cardiovascular functions, but its potential involvement in the control of vascular tone is obscure. Here, we show that both LPA (18:1) and VPC31143 (a synthetic agonist of LPA1-3 receptors) relax intact mouse thoracic aorta with similar Emax values (53.9 and 51.9% of phenylephrine-induced precontraction), although the EC50 of LPA- and VPC31143-induced vasorelaxations were different (400 vs. 15 nM, respectively). Mechanical removal of the endothelium or genetic deletion of endothelial nitric oxide synthase (eNOS) not only diminished vasorelaxation by LPA or VPC31143 but converted it to vasoconstriction. Freshly isolated mouse aortic endothelial cells expressed LPA1, LPA2, LPA4 and LPA5 transcripts. The LPA1,3 antagonist Ki16425, the LPA1 antagonist AM095, and the genetic deletion of LPA1, but not that of LPA2, abolished LPA-induced vasorelaxation. Inhibition of the phosphoinositide 3 kinase-protein kinase B/Akt pathway by wortmannin or MK-2206 failed to influence the effect of LPA. However, pharmacological inhibition of phospholipase C (PLC) by U73122 or edelfosine, but not genetic deletion of PLCε, abolished LPA-induced vasorelaxation and indicated that a PLC enzyme, other than PLCε, mediates the response. In summary, the present study identifies LPA as an endothelium-dependent vasodilator substance acting via LPA1, PLC, and eNOS.

Indexed as

AnimalsCells, CulturedEndothelial CellsIn Vitro TechniquesLysophospholipidsMiceMice, Inbred C57BLMice, KnockoutNitric Oxide Synthase Type IIIReceptors, Lysophosphatidic AcidType C PhospholipasesVasodilationlysophosphatidic acidLysophospholipidsNitric Oxide Synthase Type IIIReceptors, Lysophosphatidic AcidType C PhospholipasesendotheliumeNOSLPAphospholipase Cvasorelaxation

Identifiers

PMID24249637
PMCPMC3898652
OpenAlexW2129127131

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.