Evidence map›Paper›PMID 9782120›Full record

ArticleThe Journal of experimental medicine1998

Neutrophil-derived 5'-adenosine monophosphate promotes endothelial barrier function via CD73-mediated conversion to adenosine and endothelial A2B receptor activation.

P F Lennon, C T Taylor, G L Stahl, S P Colgan

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

104 citing papers in PubMed, 232 citations in OpenAlex.

  1. Trial
  2. Immunoregulatory extracellular vesicles in multiple myeloma patients' peripheral blood.Extracellular vesicles and circulating nucleic acids · 2026
    Article
  3. Adenosine-mediated immune responses in inflammatory bowel disease.Frontiers in cell and developmental biology · 2024
    Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Extracellular membrane vesicles fromFrontiers in microbiology · 2022
    Article
  11. Article
  12. Article
  13. Targeting of G-protein coupled receptors in sepsis.Pharmacology & therapeutics · 2020
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. The Hypoxia-Adenosine Link during Intestinal Inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2018
    Review
  19. Article
  20. Review

44 more citing papers are in PubMed but not listed here.

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.

P F LennonCenter for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesia, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.
C T Taylor
G L Stahl
S P Colgan
Harvard University · USBrigham and Women's Hospital · US

Funding

ROLE OF EPITHELIA IN ISCHEMIA/REPERFUSION INJURYR01DK050189 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI COLGAN, SEAN P · 2000 to 2024
$5.0M
MECHANISMS OF COMPLEMENT INDUCED ENDOTHELIAL DYSFUNCTIONR01HL056086 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI STAHL, GREGORY L · 1996 to 2014
$5.0M
Hypoxia, HIF, and Mucosal InflammationR37DK050189 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI COLGAN, SEAN P · 2010 to 2019
$4.1M
MECHANISMS OF COMPLEMENT INDUCED MYOCARDIAL ISCHEMIAR01HL052886 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI STAHL, GREGORY L · 1999 to 2007
$3.5M
Mechanisms of complement induced endothelial dysfunctionR56HL056086 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI STAHL, GREGORY L · 2009 to 2009
$445k
EPITHELIA AND ISCHEMIA/REPERFUSION INJURYR29DK050189 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI COLGAN, SEAN P · 1995 to 1999
–
NEUTROPHIL INFLUENCES ON ENDOTHELIAL PERMEABILITYK08HL003688 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI LENNON, PAUL F · 1997 to 1998
–
IMPACT OF HYPOXIA ON EPITHELIAL FUNCTIONF32DK009699 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI TAYLOR, CORMAC T · 1997 to 1998
–
NHLBI NIH HHS KO8 HL03688-01NHLBI NIH HHS R01 HL052886NHLBI NIH HHS R01 HL056086NHLBI NIH HHS R56 HL056086NIDDK NIH HHS DK09699NIDDK NIH HHS DK50189NIDDK NIH HHS F32 DK009699NIDDK NIH HHS R01 DK050189NIDDK NIH HHS R29 DK050189NIDDK NIH HHS R37 DK050189
6 · The paper itself

Abstract

During episodes of inflammation, polymorphonuclear leukocyte (PMN) transendothelial migration has the potential to disturb vascular barrier function and give rise to intravascular fluid extravasation and edema. However, little is known regarding innate mechanisms that dampen fluid loss during PMN-endothelial interactions. Using an in vitro endothelial paracellular permeability model, we observed a PMN-mediated decrease in endothelial paracellular permeability. A similar decrease was elicited by cell-free supernatants from activated PMN (FMLP 10(-6) M), suggesting the presence of a PMN-derived soluble mediator(s). Biophysical and biochemical analysis of PMN supernatants revealed a role for PMN-derived 5'-adenosine monophosphate (AMP) and its metabolite, adenosine, in modulation of endothelial paracellular permeability. Supernatants from activated PMN contained micromolar concentrations of bioactive 5'-AMP and adenosine. Furthermore, exposure of endothelial monolayers to authentic 5'-AMP and adenosine increased endothelial barrier function more than twofold in both human umbilical vein endothelial cells and human microvascular endothelial cells. 5'-AMP bioactivity required endothelial CD73-mediated conversion of 5'-AMP to adenosine via its 5'-ectonucleotidase activity. Decreased endothelial paracellular permeability occurred through adenosine A2B receptor activation and was accompanied by a parallel increase in intracellular cAMP. We conclude that activated PMN release soluble mediators, such as 5'-AMP and adenosine, that promote endothelial barrier function. During inflammation, this pathway may limit potentially deleterious increases in endothelial paracellular permeability and could serve as a basic mechanism of endothelial resealing during PMN transendothelial migration.

Indexed as

Capillary Permeability5'-NucleotidaseAdenosineAdenosine MonophosphateCells, CulturedCyclic AMPEndothelium, VascularHumansNeutrophilsReceptors, Purinergic P15'-NucleotidaseAdenosineAdenosine MonophosphateCyclic AMPReceptors, Purinergic P1

Identifiers

PMID9782120
PMCPMC2213403
OpenAlexW2133068443

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.