Evidence map›Paper›PMID 14744991›Full record

ArticleThe Journal of experimental medicine2004

Insulin induces the release of vasodilator compounds from platelets by a nitric oxide-G kinase-VAMP-3-dependent pathway.

Voahanginirina Randriamboavonjy, Jürgen Schrader, Rudi Busse, Ingrid Fleming

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

22 citing papers in PubMed, 67 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Phosphoproteomic response of cardiac endothelial cells to ischemia and ultrasound.Biochimica et biophysica acta. Proteins and proteomics · 2021
    Article
  6. Article
  7. Review
  8. Article
  9. The eNOS signalosome and its link to endothelial dysfunction.Pflugers Archiv : European journal of physiology · 2016
    Review
  10. Article
  11. Article
  12. Article
  13. Signaling during platelet adhesion and activation.Arteriosclerosis, thrombosis, and vascular biology · 2010
    Review
  14. Altered nitric oxide/cGMP platelet signaling pathway in platelets from patients with acute coronary syndromes.Clinical research in cardiology : official journal of the German Cardiac Society · 2010
    Article
  15. Molecular mechanisms underlying the activation of eNOS.Pflugers Archiv : European journal of physiology · 2010
    Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Nitric oxide regulates endocytosis by S-nitrosylation of dynamin.Proceedings of the National Academy of Sciences of the United States of America · 2006
    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

4 authors at 2 institutions in 1 country.

Voahanginirina RandriamboavonjyInstitut für Kardiovaskuläre Physiologie, Klinikum der J.W.Goethe-Universität, D-60590 Frankfurt am Main, Germany.
Jürgen Schrader
Rudi Busse
Ingrid Fleming
Goethe University Frankfurt · DEHeinrich Heine University Düsseldorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Insulin-induced vasodilatation is sensitive to nitric oxide (NO) synthase (NOS) inhibitors. However, insulin is unable to relax isolated arteries or to activate endothelial NOS in endothelial cells. Since insulin can enhance platelet endothelial NOS activity, we determined whether insulin-induced vasodilatation can be attributed to a NO-dependent, platelet-mediated process. Insulin failed to relax endothelium-intact rings of porcine coronary artery. The supernatant from insulin-stimulated human platelets induced complete relaxation, which was prevented by preincubation of platelets with a NOS inhibitor, the soluble guanylyl cyclase inhibitor, NS 2028, or the G kinase inhibitor, KT 5823, and was abolished by an adenosine A2A receptor antagonist. Insulin induced the release of adenosine trisphosphate (ATP), adenosine, and serotonin from platelet-dense granules in a NO-dependent manner. This response was not detected using insulin-stimulated platelets from endothelial NOS-/- mice, although a NO donor elicited ATP release. Insulin-induced ATP release from human platelets correlated with the association of syntaxin 2 with the vesicle-associated membrane protein 3 but was not associated with the activation of alphaIIbbeta3 integrin. Thus, insulin elicits the release of vasoactive concentrations of ATP and adenosine from human platelets via a NO-G kinase-dependent signaling cascade. The mechanism of dense granule secretion involves the G kinase-dependent association of syntaxin 2 with vesicle-associated membrane protein 3.

Indexed as

AdenosineAdenosine TriphosphateBlood PlateletsCarbazolesEndothelium, VascularEnzyme InhibitorsGuanylate CyclaseHumansIndolesInsulinIn Vitro TechniquesNitric OxideOxadiazolesOxazinesProtein Kinase InhibitorsSerotoninAdenosineAdenosine TriphosphateCarbazolesEnzyme InhibitorsGuanylate CyclaseIndolesInsulinKT 5823Nitric OxideNS 2028OxadiazolesOxazinesProtein Kinase InhibitorsSerotonin

Identifiers

PMID14744991
PMCPMC2211801
OpenAlexW2124895037

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.