Evidence map›Paper›PMID 11927609›Full record

ArticleThe Journal of cell biology2002

PECAM-1 (CD31) regulates a hydrogen peroxide-activated nonselective cation channel in endothelial cells.

Guangju Ji, Christopher D O'Brien, Morris Feldman, Yefim Manevich, Poay Lim, Jing Sun, Steven M Albelda, Michael I Kotlikoff

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

15 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
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  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. CCL2 disrupts the adherens junction: implications for neuroinflammation.Laboratory investigation; a journal of technical methods and pathology · 2012
    Article
  9. Involvement of endothelial-derived relaxing factors in the regulation of cerebral blood flow.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2011
    Review
  10. Article
  11. SHP-2 phosphatase activity is required for PECAM-1-dependent cell motility.American journal of physiology. Cell physiology · 2010
    Article
  12. Article
  13. Review
  14. Article
  15. 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

8 authors at 3 institutions in 1 country.

Guangju JiDivision of Pulmonary, Allergy, and Critical Care Medicine, University of Pennsylvania School of Medicine, Philadelphia 19104, USA.
Christopher D O'Brien
Morris Feldman
Yefim Manevich
Poay Lim
Jing Sun
Steven M Albelda
Michael I Kotlikoff
Pulmonary and Allergy Associates · USCornell University · USUniversity of Pennsylvania · US

Funding

PECAM AND CALCIUM SIGNALING AND TRANSMIGRATIONR01HL049591 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI ALBELDA, STEVEN MARK · 1993 to 2002
$856k
MECHANISMS OF PECAM-1 SIGNALING IN ENDOTHELIAL CELLSK08HL004248 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI O'BRIEN, CHRISTOPHER D · 2000 to 2002
$291k
NHLBI NIH HHS HL04248NHLBI NIH HHS HL49591
6 · The paper itself

Abstract

Hydrogen peroxide (H2O2) released by neutrophils is an important mediator of endothelial cell (EC) injury and vascular inflammation via its effect on EC-free Ca2+, [Ca2+]i. Although the underlying mechanisms are not well understood, platelet endothelial cell adhesion molecule (PECAM)-1/CD-31 is a critical modulator of neutrophil-EC transmigration. PECAM-1 is also known to regulate EC calcium signals and to undergo selective tyrosine phosphorylation. Here, we report that PECAM-1 molecules transduce EC responses to hydrogen peroxide. In human umbilical vein EC and REN cells (a PECAM-1-negative EC-like cell line) stably transfected with PECAM-1 (RHP), noncytolytic H2O2 exposure (100-200 microM H2O2) activated a calcium-permeant, nonselective cation current, and a transient rise in [Ca2+]i of similar time course. Neither response was observed in untransfected REN cells, and H2O2-evoked cation current was ablated in REN cells transfected with PECAM-1 constructs mutated in the cytoplasmic tyrosine-containing domain. The PECAM-dependent H2O2 current was inhibited by dialysis of anti-PECAM-1 cytoplasmic domain antibodies, required Src family tyrosine kinase activity, was independent of inositol trisphosphate receptor activation, and required only an intact PECAM-1 cytoplasmic domain. PECAM-1-dependent H2O2 currents and associated [Ca2+]i transients may play a significant role in regulating neutrophil-endothelial interaction, as well as in oxidant-mediated endothelial response and injury.

Indexed as

CalciumCalcium ChannelsCation Transport ProteinsCell LineCytoplasmEndothelium, VascularHumansHydrogen PeroxideInositol 1,4,5-Trisphosphate ReceptorsLanthanumMembrane PotentialsOxidantsPatch-Clamp TechniquesPhosphatidylinositolsPhosphorylationPlatelet Endothelial Cell Adhesion Molecule-1CalciumCalcium ChannelsCation Transport ProteinsHydrogen PeroxideInositol 1,4,5-Trisphosphate ReceptorsITPR1 protein, humanLanthanumOxidantsPhosphatidylinositolsPlatelet Endothelial Cell Adhesion Molecule-1Receptors, Cytoplasmic and Nuclearsrc-Family KinasesTyrosine

Identifiers

PMID11927609
PMCPMC2173260
OpenAlexW2116523681

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.