Evidence map›Paper›PMID 24477234›Full record

ArticleAmerican journal of physiology. Cell physiology2014

Intermittent hypoxia-induced endothelial barrier dysfunction requires ROS-dependent MAP kinase activation.

Vladislav V Makarenko, Peter V Usatyuk, Guoxiang Yuan, May M Lee, Jayasri Nanduri, Viswanathan Natarajan, Ganesh K Kumar, Nanduri R Prabhakar

Abstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
6.0field-weighted citation impact, top 4% 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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Vladislav V MakarenkoUniversity of Chicago, Institute For Integrative Physiology and Center for Systems Biology of O2 Sensing, Chicago, Illinois; and.
Peter V Usatyuk
Guoxiang Yuan
May M Lee
Jayasri Nanduri
Viswanathan Natarajan
Ganesh K Kumar
Nanduri R Prabhakar
Center for Systems Biology · USUniversity of Illinois Chicago · USUniversity of Chicago · US

Funding

Tissue Culture Biomechanical CoreP01HL058064 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI LAL, RATNESHWAR · 1998 to 2012
$27.8M
Integrative Consequences of HypoxiaP01HL090554 · NHLBI · UNIVERSITY OF CHICAGO · PI PRABHAKAR, NANDURI R · 2008 to 2017
$21.4M
Re-Engineering Translational Research at the University of ChicagoUL1TR000430 · NCATS · UNIVERSITY OF CHICAGO · PI SOLWAY, JULIAN · 2012 to 2016
$20.2M
Therapeutic Potential of FTY720 Analogues in Lung InjuryP01HL098050 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI NATARAJAN, VISWANATHAN · 2011 to 2015
$10.9M
Consequences of Neonatal HypoxiaR01HL076537 · NHLBI · UNIVERSITY OF CHICAGO · PI PRABHAKAR, NANDURI R · 2005 to 2009
$1.8M
NCATS NIH HHS UL1 TR000430NHLBI NIH HHS P01 HL058064NHLBI NIH HHS P01 HL090554NHLBI NIH HHS P01 HL098050NHLBI NIH HHS P01-HL-58064NHLBI NIH HHS P01-HL-90554NHLBI NIH HHS R01 HL076537NHLBI NIH HHS R01-HL-76537
6 · The paper itself

Abstract

The objective of the present study was to determine the impact of simulated apnea with intermittent hypoxia (IH) on endothelial barrier function and assess the underlying mechanism(s). Experiments were performed on human lung microvascular endothelial cells exposed to IH-consisting alternating cycles of 1.5% O2 for 30s followed by 20% O2 for 5 min. IH decreased transendothelial electrical resistance (TEER) suggesting attenuated endothelial barrier function. The effect of IH on TEER was stimulus dependent and reversible after reoxygenation. IH-exposed cells exhibited stress fiber formation and redistribution of cortactin, vascular endothelial-cadherins, and zona occludens-1 junction proteins along with increased intercellular gaps at cell-cell boundaries. Extracellular signal-regulated kinase (ERK) and c-jun NH2-terminal kinase (JNK) were phosphorylated in IH-exposed cells. Inhibiting either ERK or JNK prevented the IH-induced decrease in TEER and the reorganization of the cytoskeleton and junction proteins. IH increased reactive oxygen species (ROS) levels, and manganese (III) tetrakis (1-methyl-4-pyridyl) porphyrin pentachloride, a membrane-permeable antioxidant, prevented ERK and JNK phosphorylation as well as IH-induced changes in endothelial barrier function. These results demonstrate that IH via ROS-dependent activation of MAP kinases leads to reorganization of cytoskeleton and junction proteins resulting in endothelial barrier dysfunction.

Indexed as

Cells, CulturedCytoskeletonElectric ImpedanceEndothelial CellsEnzyme ActivationGene Expression Regulation, EnzymologicHumansHypoxiaIntercellular JunctionsLungMitogen-Activated Protein Kinase KinasesOxidative StressOxygenPhosphorylationReactive Oxygen SpeciesTime FactorsMitogen-Activated Protein Kinase KinasesOxygenReactive Oxygen Speciescytoskeleton proteinsjunction proteinsmicrovascular endothelial cellsoxidative stress

Identifiers

PMID24477234
PMCPMC3989715
OpenAlexW2158745827

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.