Evidence map›Paper›PMID 21653902›Full record

ArticleAmerican journal of physiology. Cell physiology2011

Leukocyte rolling and adhesion both contribute to regulation of microvascular permeability to albumin via ligation of ICAM-1.

Ronen Sumagin, Julia M Kuebel, Ingrid H Sarelius

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

30 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Deciphering albumin-directed drug delivery by imaging.Advanced drug delivery reviews · 2022
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Extracellular vesicles: new players in regulating vascular barrier function.American journal of physiology. Heart and circulatory physiology · 2020
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Endothelial MAPKs Direct ICAM-1 Signaling to Divergent Inflammatory Functions.Journal of immunology (Baltimore, Md. : 1950) · 2017
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Ronen SumaginDepartment of Pharmacology and Physiology, University of Rochester, New York 14642, USA.
Julia M Kuebel
Ingrid H Sarelius
University of Rochester · US

Funding

VASCULAR RELATIONS OF BLOOD CELLS AND PROTEINSP01HL018208 · NHLBI · UNIVERSITY OF ROCHESTER · PI WAUGH, RICHARD E · 1985 to 2014
$24.7M
Inflammatory Mechanisms in Arterioles and VenulesR01HL075186 · NHLBI · UNIVERSITY OF ROCHESTER · PI SARELIUS, INGRID H · 2003 to 2006
$1.5M
NHLBI NIH HHS HL-18208NHLBI NIH HHS HL-75186
6 · The paper itself

Abstract

Activated neutrophils interacting with the vessel wall can alter vascular permeability to macromolecules such as albumin via release of various secretion products that induce changes in the endothelial monolayer. In the current work we used cremaster microvessels of anesthetized mice to show that, in addition to this paracrine mechanism, leukocyte ligation of endothelial ICAM-1 directly activates endothelial cell (EC) signaling, altering EC permeability to albumin [i.e., solute permeability (P(s))]. We show that antibody cross-linking of surface ICAM-1 in intact microvessels is sufficient to increase P(s) even in the absence of interacting leukocytes. Unstimulated arterioles do not support leukocyte-EC interactions, but despite this, antibody ligation of ICAM-1 in these vessels induced a twofold increase in P(s). Similarly, in venules that were depleted of interacting neutrophils, P(s) was decreased to below resting levels and was restored by ligation of ICAM-1. Use of function-blocking antibodies to separately block leukocyte rolling or adhesion under unstimulated or TNF-α-activated conditions established that both rolling and adhered leukocytes contribute to P(s) regulation in situ. Both rolling and adhesion activated EC-dependent signaling mechanisms that increased P(s). ICAM-1 ligation with primary antibody alone or primary followed by secondary antibodies showed that regulation of P(s) is directly dependent on the degree of ICAM-1 clustering. Under physiological versus inflamed conditions, respectively, this ICAM-1 clustering-dependent regulation of P(s) switches from PKC dependent and Src independent to Src dependent and PKC independent. This study thus identifies a new mechanism by which antiadhesion treatment may constitute a potential therapy for tissue edema.

Indexed as

AlbuminsAnimalsCapillary PermeabilityCell AdhesionGene Expression RegulationIntercellular Adhesion Molecule-1Leukocyte RollingLeukocytesMiceMice, KnockoutReceptors, Tumor Necrosis FactorSignal TransductionTumor Necrosis Factor-alphaAlbuminsIntercellular Adhesion Molecule-1Receptors, Tumor Necrosis FactorTumor Necrosis Factor-alpha

Identifiers

PMID21653902
PMCPMC3191564
OpenAlexW2010849442

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.