Evidence map›Paper›PMID 24477600›Full record

ArticleJournal of cellular physiology2014

Adenosine regulates the proinflammatory signaling function of thrombin in endothelial cells.

Seyed Mahdi Hassanian, Peyman Dinarvand, Alireza R Rezaie

Abstract read
In one paragraph

Article in Journal of cellular physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
5.5field-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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.

  1. Pooled it
  2. Article
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  10. Vactosertib potently improves anti-tumor properties of 5-FU for colon cancer.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2023
    Article
  11. Observational
  12. Article
  13. Article
  14. Review
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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

3 authors at 2 institutions in 2 countries.

Seyed Mahdi HassanianEdward A. Doisy Department of Biochemistry and Molecular Biology, Saint Louis University School of Medicine, St. Louis, Missouri.
Peyman Dinarvand
Alireza R Rezaie
Saint Louis University · USSaint Louis University · ES

Funding

Protease Activated Receptor Signaling by Coagulation ProteasesR01HL101917 · NHLBI · SAINT LOUIS UNIVERSITY · PI Lijun Xia · 2010 to 2026
$6.6M
Serpin Regulation of Coagulation ProteasesR01HL062565 · NHLBI · SAINT LOUIS UNIVERSITY · PI REZAIE, ALIREZA R. · 1999 to 2020
$6.2M
Molecular Basis of Coagulation Protease SpecificityR01HL068571 · NHLBI · SAINT LOUIS UNIVERSITY · PI REZAIE, ALIREZA R. · 2002 to 2010
$3.1M
NHLBI NIH HHS HL 101917NHLBI NIH HHS HL 68571NHLBI NIH HHS R01 HL062565NHLBI NIH HHS R01 HL068571NHLBI NIH HHS R01 HL101917
6 · The paper itself

Abstract

The plasma level of the regulatory metabolite adenosine increases during the activation of coagulation and inflammation. Here we investigated the effect of adenosine on modulation of thrombin-mediated proinflammatory responses in HUVECs. We found that adenosine inhibits the barrier-disruptive effect of thrombin in HUVECs by a concentration-dependent manner. Analysis of cell surface expression of adenosine receptors revealed that A2A and A2B are expressed at the highest level among the four receptor subtypes (A2B  > A2A  > A1  > A3 ) on HUVECs. The barrier-protective effect of adenosine in response to thrombin was recapitulated by the A2A specific agonist, CGS 21680, and abrogated both by the siRNA knockdown of the A2A receptor and by the A2A -specific antagonists, ZM-241385 and SCH-58261. The thrombin-induced RhoA activation and its membrane translocation were both inhibited by adenosine in a cAMP-dependent manner, providing a molecular mechanism through which adenosine exerts a barrier-protective function. Adenosine also inhibited thrombin-mediated activation of NF-κB and decreased adhesion of monocytic THP-1 cells to stimulated HUVECs via down-regulation of expression of cell surface adhesion molecules, VCAM-1, ICAM-1, and E-selectin. Moreover, adenosine inhibited thrombin-induced elevated expression of proinflammatory cytokines, IL-6 and HMGB-1; and chemokines, MCP-1, CXCL-1, and CXCL-3. Taken together, these results suggest that adenosine may inhibit thrombin-mediated proinflammatory signaling responses, thereby protecting the endothelium from injury during activation of coagulation and inflammation.

Indexed as

Blood CoagulationSignal TransductionAdenosineAdenosine A2 Receptor AgonistsAdenosine A2 Receptor AntagonistsCapillary PermeabilityCell AdhesionCells, CulturedCoculture TechniquesCyclic AMPDose-Response Relationship, DrugEnzyme ActivationE-SelectinHumansHuman Umbilical Vein Endothelial CellsInflammationAdenosineAdenosine A2 Receptor AgonistsAdenosine A2 Receptor AntagonistsCyclic AMPE-SelectinICAM1 protein, humanInflammation MediatorsIntercellular Adhesion Molecule-1NF-kappa BReceptor, Adenosine A2AReceptor, Adenosine A2BrhoA GTP-Binding ProteinRHOA protein, humanSELE protein, humanThrombinVascular Cell Adhesion Molecule-1

Identifiers

PMID24477600
PMCPMC4037378
OpenAlexW1928947060

What OpenQuestion holds

Textmetadata
LicenceTDM
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.