Evidence map›Paper›PMID 22159995›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2012

Prostacyclin receptor-mediated ATP release from erythrocytes requires the voltage-dependent anion channel.

Meera Sridharan, Elizabeth A Bowles, Jennifer P Richards, Medina Krantic, Katie L Davis, Kristine A Dietrich, Alan H Stephenson, Mary L Ellsworth, Randy S Sprague

Abstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.8field-weighted citation impact, top 9% 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, 58 citations in OpenAlex.

  1. Trial
  2. Article
  3. The impact of nebulized epoprostenol and iloprost on hemoglobin oxygen affinity: an ex vivo experiment.American journal of physiology. Lung cellular and molecular physiology · 2022
    Article
  4. Review
  5. Review
  6. Review
  7. Alteration of purinergic signaling in diabetes: Focus on vascular function.Journal of molecular and cellular cardiology · 2020
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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

9 authors at 1 institution in 1 country.

Meera SridharanDepartment of Pharmacological and Physiological Science, Saint Louis University School of Medicine, Saint Louis, Missouri, MO 63104, USA. meerasrid@gmail.com
Elizabeth A Bowles
Jennifer P Richards
Medina Krantic
Katie L Davis
Kristine A Dietrich
Alan H Stephenson
Mary L Ellsworth
Randy S Sprague
Saint Louis University · US

Funding

Microvascular O2 Delivery: Impact of Erythrocyte-Released ATPR33HL089094 · NHLBI · SAINT LOUIS UNIVERSITY · PI ELLSWORTH, MARY L · 2007 to 2009
$1.6M
NHLBI NIH HHS HL-089094
6 · The paper itself

Abstract

Erythrocytes have been implicated as controllers of vascular caliber by virtue of their ability to release the vasodilator ATP in response to local physiological and pharmacological stimuli. The regulated release of ATP from erythrocytes requires activation of a signaling pathway involving G proteins (G(i) or G(s)), adenylyl cyclase, protein kinase A, and the cystic fibrosis transmembrane conductance regulator as well as a final conduit through which this highly charged anion exits the cell. Although pannexin 1 has been shown to be the final conduit for ATP release from human erythrocytes in response to reduced oxygen tension, it does not participate in transport of ATP following stimulation of the prostacyclin (IP) receptor in these cells, which suggests that an additional protein must be involved. Using antibodies directed against voltage-dependent anion channel (VDAC)1, we confirm that this protein is present in human erythrocyte membranes. To address the role of VDAC in ATP release, two structurally dissimilar VDAC inhibitors, Bcl-x(L) BH4(4-23) and TRO19622, were used. In response to the IP receptor agonists, iloprost and UT-15C, ATP release was inhibited by both VDAC inhibitors although neither iloprost-induced cAMP accumulation nor total intracellular ATP concentration were altered. Together, these findings support the hypothesis that VDAC is the ATP conduit in the IP receptor-mediated signaling pathway in human erythrocytes. In addition, neither the pannexin inhibitor carbenoxolone nor Bcl-x(L) BH4(4-23) attenuated ATP release in response to incubation of erythrocytes with the β-adrenergic receptor agonist isoproterenol, suggesting the presence of yet another channel for ATP release from human erythrocytes.

Indexed as

Adenosine TriphosphateAdrenergic beta-AgonistsAdultAnimalsAntihypertensive Agentsbcl-X ProteinCarbenoxoloneConnexinsCyclic AMPEpoprostenolErythrocyte MembraneFemaleHumansIloprostIsoproterenolMaleAdenosine TriphosphateAdrenergic beta-AgonistsAntihypertensive AgentsBCL2L1 protein, humanbcl-X ProteinCarbenoxoloneConnexinsCyclic AMPEpoprostenolIloprostIsoproterenolNerve Tissue ProteinsPANX1 protein, humanPTGIR protein, humanReceptors, EpoprostenolReceptors, ProstaglandintreprostinilVasodilator AgentsVDAC1 protein, humanVoltage-Dependent Anion Channel 1

Identifiers

PMID22159995
PMCPMC3353798
OpenAlexW2113728300

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.