Evidence map›Paper›PMID 21864543›Full record

ReviewMicrovascular research2012

Neutrophil transmigration, focal adhesion kinase and endothelial barrier function.

Sarah Y Yuan, Qiang Shen, Robert R Rigor, Mack H Wu

Abstract readReview
In one paragraph

Review in Microvascular research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

40 citing papers in PubMed, 82 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Genetic or therapeutic disruption of the Reelin/Apoer2 signaling pathway improves inflammatory arthritis outcomes.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. The Gut-Lung Axis in Systemic Inflammation. Role of Mesenteric Lymph as a Conduit.American journal of respiratory cell and molecular biology · 2021
    Review
  18. Article
  19. Article
  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

4 authors at 1 institution in 1 country.

Sarah Y YuanDivision of Research, Department of Surgery, University of California at Davis School of Medicine, Sacramento, CA 95817, USA.
Qiang Shen
Robert R Rigor
Mack H Wu
University of California, Davis · US

Funding

Microvascular Barrier Dysfunction in Thermal TraumaR01HL070752 · NHLBI · UNIVERSITY OF SOUTH FLORIDA · PI YUAN, SARAH Y · 2002 to 2018
$4.7M
NEUTROPHIL DEPENDENT REGULATION OF VENULAR PERMEABILITYR01HL061507 · NHLBI · UNIVERSITY OF SOUTH FLORIDA · PI YUAN, SARAH Y · 1999 to 2011
$3.4M
Disintegrin Metalloprotease and Endothelial PermeabilityR01GM097270 · NIGMS · UNIVERSITY OF SOUTH FLORIDA · PI YUAN, SARAH Y · 2011 to 2020
$2.3M
Microvascular Permeability and Matrix Fibrinogen Degradation in TraumaR01HL096640 · NHLBI · UNIVERSITY OF SOUTH FLORIDA · PI WU, MACK H · 2009 to 2013
$1.9M
PKC Isoenzymes Diabetic Microvascular HyperpermeabilityR01HL084542 · NHLBI · UNIVERSITY OF SOUTH FLORIDA · PI YUAN, SARAH Y · 2006 to 2010
$1.9M
VEGF Regulation of Microvascular PermeabilityR01HL073324 · NHLBI · UNIVERSITY OF CALIFORNIA DAVIS · PI WU, MACK H · 2004 to 2008
$1.6M
NHLBI NIH HHS HL061507NHLBI NIH HHS HL070752NHLBI NIH HHS HL073324NHLBI NIH HHS HL084542NHLBI NIH HHS HL096640NHLBI NIH HHS R01 HL061507NHLBI NIH HHS R01 HL070752NHLBI NIH HHS R01 HL073324NHLBI NIH HHS R01 HL084542NHLBI NIH HHS R01 HL096640NIGMS NIH HHS R01 GM097270
6 · The paper itself

Abstract

Neutrophil activation is an essential component of innate immune defense against infection and injury. In response to inflammatory stimulation, circulating neutrophils undergo a series of dynamic and metabolic changes characterized by β2-intergrin mediated adhesion to microvascular endothelium and subsequent transendothelial migration. During this process, neutrophils release granular contents containing digestive enzymes and produce cytotoxic agents such as reactive oxygen species and cytokines. These products target endothelial barriers inducing phosphorylation-triggered junction dissociation, actin stress fiber formation, and actomyosin contraction, manifest as paracellular hyperpermeability. Endothelial cell-matrix focal adhesions play an integral role in this process by providing structural support for endothelial conformational changes that facilitate neutrophil transmigration, as well as by recruiting intracellular molecules that constitute the hyperpermeability signaling cascades. As a central connector of the complex signaling network, focal adhesion kinase (FAK) is activated following neutrophil adhesion, and further mediates the reorganization of endothelial integrin-matrix attachments in a pattern coordinating with cytoskeleton contraction and junction opening. In this review, we present recent experimental evidence supporting the importance of FAK in neutrophil-dependent regulation of endothelial permeability. The discussion focuses on the mechanisms by which neutrophils activate FAK and its downstream effects on endothelial barriers.

Indexed as

Capillary PermeabilityNeutrophil ActivationTransendothelial and Transepithelial MigrationAnimalsCell AdhesionEndothelial CellsEnzyme ActivationFocal Adhesion Protein-Tyrosine KinasesFocal AdhesionsHumansNeutrophilsSignal TransductionFocal Adhesion Protein-Tyrosine Kinases

Identifiers

PMID21864543
PMCPMC3232323
OpenAlexW2094555042

What OpenQuestion holds

Textmetadata
LicenceTDM
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.