Evidence map›Paper›PMID 23288152›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2013

Claudin-5 controls intercellular barriers of human dermal microvascular but not human umbilical vein endothelial cells.

Martin S Kluger, Paul R Clark, George Tellides, Volker Gerke, Jordan S Pober

Open access · greenAbstract readComparative Study
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
5.1field-weighted citation impact, top 5% 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

57 citing papers in PubMed, 86 citations in OpenAlex.

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  15. The Expression of Proto-OncogeneInternational journal of molecular sciences · 2022
    Review
  16. ArhGEF12 activates Rap1A and not RhoA in human dermal microvascular endothelial cells to reduce tumor necrosis factor-induced leak.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    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

5 authors at 1 institution in 1 country.

Martin S KlugerDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06519, USA. martin.kluger@yale.edu
Paul R Clark
George Tellides
Volker Gerke
Jordan S Pober
Yale University · US

Funding

IMMUNOHEMATOLOGY/TRANSFUSION MEDICINE RESEARCH TRAININGT32HL007974 · NHLBI · YALE UNIVERSITY · PI JEANNE E HENDRICKSON, Diane S Krause · 2001 to 2026
$8.1M
PROTEINS OF THE ENDOTHELIAL CELL SURFACER01HL036003 · NHLBI · YALE UNIVERSITY · PI KLUGER, MARTIN S, POBER, JORDAN S · 1985 to 2015
$5.7M
NHLBI NIH HHS 2R01-HL036003NHLBI NIH HHS R01 HL036003NHLBI NIH HHS T32 HL007974
6 · The paper itself

Abstract

objectiveTo assess the role claudin-5, an endothelial cell (EC) tight junction protein, plays in establishing basal permeability levels in humans by comparing claudin-5 expression levels in situ and analyzing junctional organization and function in 2 widely used models of cultured ECs, namely human dermal microvascular (HDM)ECs and human umbilical vein (HUV)ECs. METHODS AND

resultsBy immunofluorescence microscopy, ECs more highly express claudin-5 (but equivalently express vascular endothelial-cadherin) in human dermal capillaries versus postcapillary venules and in umbilical and coronary arteries versus veins, correlating with known segmental differences in tight junction frequencies and permeability barriers. Postconfluent cultured HDMECs express more claudin-5 (but equivalent vascular endothelial-cadherin) and show higher transendothelial electric resistance and lower macromolecular flux than similarly cultured HUVECs. HDMEC junctions are more complex by transmission electron microscopy and show more continuous claudin-5 immunofluorescence than HUVEC junctions. Calcium chelation or dominant negative vascular endothelial-cadherin overexpression decreases transendothelial electric resistance and disrupts junctions in HUVECs, but not in HDMECs. Claudin-5 overexpression in HUVECs fails to increase transendothelial electric resistance or claudin-5 continuity, whereas claudin-5 knockdown in HDMECs, but not in HUVECs, reduces transendothelial electric resistance and increases antibody accessibility to junctional proteins.

conclusionsClaudin-5 expression and junctional organization control HDMEC and arteriolar-capillary paracellular barriers, whereas HUVEC and venular junctions use vascular endothelial-cadherin.

Indexed as

Capillary PermeabilityAntigens, CDCadherin 5CadherinsCalciumCells, CulturedChelating AgentsClaudin-5Electric ImpedanceEndothelial CellsGene Knockdown TechniquesHumansHuman Umbilical Vein Endothelial CellsMicroscopy, Electron, TransmissionMicroscopy, FluorescenceMicrovesselsAntigens, CDCadherin 5CadherinsCalciumChelating AgentsClaudin-5CLDN5 protein, human

Identifiers

PMID23288152
PMCPMC3655806
OpenAlexW2136491609

What OpenQuestion holds

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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.