Evidence map›Paper›PMID 19122172›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2009

Fibrinogen-gamma C-terminal fragments induce endothelial barrier dysfunction and microvascular leak via integrin-mediated and RhoA-dependent mechanism.

Mingzhang Guo, Dayle Daines, Jing Tang, Qiang Shen, Rachel M Perrin, Yoshikazu Takada, Sarah Y Yuan, Mack H Wu

Open access · greenAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

20 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. Calpain Promotes LPS-induced Lung Endothelial Barrier Dysfunction via Cleavage of Talin.American journal of respiratory cell and molecular biology · 2023
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  13. Review
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  15. Alzheimer's disease peptide beta-amyloid interacts with fibrinogen and induces its oligomerization.Proceedings of the National Academy of Sciences of the United States of America · 2010
    Article
  16. Article
  17. Article
  18. Review
  19. Article
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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 1 institution in 1 country.

Mingzhang GuoDivision of Research, Department of Surgery, University of California Davis School of Medicine, Sacramento, CA 95817, USA.
Dayle Daines
Jing Tang
Qiang Shen
Rachel M Perrin
Yoshikazu Takada
Sarah Y Yuan
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
VEGF Regulation of Microvascular PermeabilityR01HL073324 · NHLBI · UNIVERSITY OF CALIFORNIA DAVIS · PI WU, MACK H · 2004 to 2008
$1.6M
NHLBI NIH HHS HL-061507NHLBI NIH HHS HL-070752NHLBI NIH HHS HL-073324NHLBI NIH HHS R01 HL061507NHLBI NIH HHS R01 HL070752NHLBI NIH HHS R01 HL073324
6 · The paper itself

Abstract

objectivesThe purposes of this study were to characterize the direct effect of the C-terminal fragment of fibrinogen gamma chain (gammaC) on microvascular endothelial permeability and to examine its molecular mechanism of action. METHODS AND

resultsIntravital microscopy was performed to measure albumin extravasation in intact mesenteric microvasculature, followed by quantification of hydraulic conductivity in single perfused microvessels. Transendothelial electric resistance was measured in microvascular endothelial cells in combination with immunoblotting and immunocytochemistry. The results show that gammaC induced time- and concentration-dependent increases in protein transvascular flux and water permeability and decreases in endothelial barrier function, coupled with Rho GTPase activation, myosin light chain phosphorylation, and stress fiber formation. Depletion of RhoA via siRNA knockdown or pharmacological inhibition of RhoA signaling attenuated gammaC-induced barrier dysfunction. Imaging analyses demonstrated binding of gammaC to endothelial cells; the interaction was inhibited during blockage of the alphavbeta3 integrin. Furthermore, in vivo experiments showed that the microvascular leak response to gammaC was attenuated in integrin beta3(-/-) animals.

conclusionFibrinogen-gamma C terminus directly interacts with the microvascular endothelium causing fluid and protein leak. The endothelial response to gammaC involves an integrin receptor-mediated RhoA-dependent signaling pathway that leads to paracellular hyperpermeability.

Indexed as

Capillary PermeabilityMicrocirculationAlbuminsAmidesAnimalsDose-Response Relationship, DrugElectric ImpedanceEndothelium, VascularFibrinogenHumansIntegrin alphaVbeta3Integrin beta3MiceMice, Inbred C57BLMice, KnockoutMicroscopy, VideoAlbuminsAmidesFibrinogenfibrinogen gamma (151-411)Integrin alphaVbeta3Integrin beta3Myosin Light ChainsPeptide FragmentsProtein Kinase InhibitorsPyridinesRecombinant ProteinsrhoA GTP-Binding ProteinRNA, Small InterferingY 27632

Identifiers

PMID19122172
PMCPMC2737386
OpenAlexW2102879974

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.