Evidence map›Paper›PMID 18599597›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2008

Functional role of gap junctions in cytokine-induced leukocyte adhesion to endothelium in vivo.

Loreto P Véliz, Francisco G González, Brian R Duling, Juan C Sáez, Mauricio P Boric

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.7field-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

27 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Interaction between alveolar macrophages and epithelial cells duringFrontiers in cellular and infection microbiology · 2023
    Review
  7. KMicrocirculation (New York, N.Y. : 1994) · 2023
    Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. 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

5 authors at 1 institution in 1 country.

Loreto P VélizDepartamento de Ciencias Fisiológicas, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Av. B. O'Higgins 340, P.O. Box Casilla 114-D, Santiago, Chile.
Francisco G González
Brian R Duling
Juan C Sáez
Mauricio P Boric
Pontificia Universidad Católica de Chile · CL

Funding

Regulation of the Endothelial Cell GlycocalyxR01HL072864 · NHLBI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI DULING, BRIAN R · 2004 to 2008
$1.8M
INTERCELLULAR COMMUNICATION IN MICROVESSELSR01HL053318 · NHLBI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI DULING, BRIAN R · 1995 to 2004
$1.5M
NHLBI NIH HHS HL53318NHLBI NIH HHS HL72864
6 · The paper itself

Abstract

To assess the hypothesis that gap junctions (GJs) participate on leukocyte-endothelium interactions in the inflammatory response, we compared leukocyte adhesion and transmigration elicited by cytokine stimulation in the presence or absence of GJ blockers in the hamster cheek pouch and also in the cremaster muscle of wild-type (WT) and endothelium-specific connexin 43 (Cx43) null mice (Cx43e(-/-)). In the cheek pouch, topical tumor necrosis factor-alpha (TNF-alpha; 150 ng/ml, 15 min) caused a sustained increment in the number of leukocytes adhered to venular endothelium (LAV) and located at perivenular regions (LPV). Superfusion with the GJ blockers 18-alpha-glycyrrhetinic acid (AGA; 75 microM) or 18-beta-glycyrrhetinic acid (50 microM) abolished the TNF-alpha-induced increase in LAV and LPV; carbenoxolone (75 microM) or oleamide (100 microM) reduced LAV by 50 and 75%, respectively, and LPV to a lesser extent. None of these GJ blockers modified venular diameter, blood flow, or leukocyte rolling. In contrast, glycyrrhizin (75 microM), a non-GJ blocker analog of AGA, was devoid of effect. Interestingly, when AGA was removed 90 min after TNF-alpha stimulation, LAV started to rise at a similar rate as in control. Conversely, application of AGA 90 min after TNF-alpha reduced the number of previously adhered cells. In WT mice, intrascrotal injection of TNF-alpha (0.5 microg/0.3 ml) increased LAV (fourfold) and LPV (threefold) compared with saline-injected controls. In contrast to the observations in WT animals, TNF-alpha stimulation did not increase LAV or LPV in Cx43e(-/-) mice. These results demonstrate an important role for GJ communication in leukocyte adhesion and transmigration during acute inflammation in vivo and further suggest that endothelial Cx43 is key in these processes.

Indexed as

AnimalsCell AdhesionCell MovementConnexin 43CricetinaeCytokinesEndothelial CellsEndothelium, VascularGap JunctionsInflammationLeukocytesMaleMesocricetusMiceMice, Inbred C57BLMice, KnockoutConnexin 43CytokinesSodium RadioisotopesTumor Necrosis Factor-alpha

Identifiers

PMID18599597
PMCPMC2544495
OpenAlexW2099349590

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.