Evidence map›Paper›PMID 24414256›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2014

Protective effect of adenosine receptors against lipopolysaccharide-induced acute lung injury.

Joyce N Gonzales, Boris Gorshkov, Matthew N Varn, Marina A Zemskova, Evgeny A Zemskov, Supriya Sridhar, Rudolf Lucas, Alexander D Verin

Abstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
6.5field-weighted citation impact, top 3% 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

37 citing papers in PubMed, 60 citations in OpenAlex.

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  10. Anti-Inflammatory Metabolites in the Pathogenesis of Bacterial Infection.Frontiers in cellular and infection microbiology · 2022
    Review
  11. Review
  12. Adenosine and Inflammation: Here, There and Everywhere.International journal of molecular sciences · 2021
    Review
  13. Article
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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

8 authors at 3 institutions in 1 country.

Joyce N GonzalesAssistant Prof. of Medicine, Div. of Pulmonary and Critical Care Medicine, Georgia Regents Univ., Rm. BBR-5513, 1120 15th St., Augusta, GA 30912. JGONZALES@gru.edu.
Boris Gorshkov
Matthew N Varn
Marina A Zemskova
Evgeny A Zemskov
Supriya Sridhar
Rudolf Lucas
Alexander D Verin
Center for Vascular Biology Research · USGeorgia Regents Medical Center · USPulmonary and Critical Care Associates · US

Funding

Therapeutic Mechanisms of RhoA Inhibition In Acute Lung InjuryP01HL101902 · NHLBI · AUGUSTA UNIVERSITY · PI BLACK, STEPHEN M · 2011 to 2016
$11.2M
NHLBI NIH HHS HL101902
6 · The paper itself

Abstract

Acute lung injury and acute respiratory distress syndrome (ALI/ARDS) affect 200,000 people a year in the USA. Pulmonary vascular and specifically endothelial cell (EC) barrier compromise is a hallmark of these diseases. We have recently shown that extracellular adenosine enhances human pulmonary (EC) barrier via activation of adenosine receptors (ARs) in cell cultures. On the basis of these data, we hypothesized that activation of ARs might exert barrier-protective effects in a model of ALI/ARDS in mice. To test this hypothesis, we examined the effects of pre- and posttreatment of adenosine and 5'-N-ethylcarboxamidoadenosine (NECA), a nonselective stable AR agonist, on LPS-induced lung injury. Mice were given vehicle or LPS intratracheally followed by adenosine, NECA, or vehicle instilled via the internal jugular vein. Postexperiment cell counts, Evans Blue Dye albumin (EBDA) extravasation, levels of proteins, and inflammatory cytokines were analyzed. Harvested lungs were used for histology and myeloperoxidase studies. Mice challenged with LPS alone demonstrated an inflammatory response typical of ALI. Cell counts, EBDA extravasation, as well as levels of proteins and inflammatory cytokines were decreased in adenosine-treated mice. Histology displayed reduced infiltration of neutrophils. NECA had a similar effect on LPS-induced vascular barrier compromise. Importantly, posttreatment with adenosine or NECA recovers lung vascular barrier and reduces inflammation induced by LPS challenge. Furthermore, adenosine significantly attenuated protein degradation of A2A and A3 receptors induced by LPS. Collectively, our results demonstrate that activation of ARs protects and restores vascular barrier functions and reduces inflammation in LPS-induced ALI.

Indexed as

Acute Lung InjuryAdenosineAdenosine-5'-(N-ethylcarboxamide)AnimalsBronchoalveolar Lavage FluidCapillary PermeabilityCell CountCytokinesEndothelial CellsEndotheliumInflammationInterleukin-6LipopolysaccharidesLungMiceMice, Inbred C57BLAdenosineAdenosine-5'-(N-ethylcarboxamide)CytokinesInterleukin-6LipopolysaccharidesPurinergic P1 Receptor AgonistsReceptors, Purinergic P1Tumor Necrosis Factor-alphaacute lung injuryadenosinelipopolysaccharidepulmonary edemareceptors

Identifiers

PMID24414256
PMCPMC3949083
OpenAlexW2022682439

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.