Evidence map›Paper›PMID 25106430›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2014

Claudin 4 knockout mice: normal physiological phenotype with increased susceptibility to lung injury.

Hidenori Kage, Per Flodby, Danping Gao, Yong Ho Kim, Crystal N Marconett, Lucas DeMaio, Kwang-Jin Kim, Edward D Crandall, Zea Borok

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
5.0field-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

45 citing papers in PubMed, 77 citations in OpenAlex.

  1. Article
  2. Article
  3. Claudins in Cancer: A Current and Future Therapeutic Target.International journal of molecular sciences · 2024
    Review
  4. Article
  5. Article
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  18. Article
  19. Tight Junction Proteins and the Biology of Hepatobiliary Disease.International journal of molecular sciences · 2020
    Review
  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

9 authors at 3 institutions in 1 country.

Hidenori KageWill Rogers Institute Pulmonary Research Center, Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine.
Per FlodbyWill Rogers Institute Pulmonary Research Center, Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine.
Danping GaoWill Rogers Institute Pulmonary Research Center, Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine.
Yong Ho KimWill Rogers Institute Pulmonary Research Center, Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine.
Crystal N MarconettDepartments of Surgery and Biochemistry and Molecular Biology, Norris Comprehensive Cancer Center.
Lucas DeMaioWill Rogers Institute Pulmonary Research Center, Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine.
Kwang-Jin KimWill Rogers Institute Pulmonary Research Center, Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine, Departments of Physiology and Biophysics and Department of Pharmacology and Pharmaceutical Sciences, School of Pharmacy, University of Southern California; Department of Biomedical Engineering and.
Edward D CrandallWill Rogers Institute Pulmonary Research Center, Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine, Pathology, Keck School of Medicine, University of Southern California; Mork Family Department of Chemical Engineering and Materials Science, Viterbi School of Engineering, University of Southern California, Los Angeles, California.
Zea BorokWill Rogers Institute Pulmonary Research Center, Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine, Biochemistry and Molecular Biology, Norris Comprehensive Cancer Center, zborok@med.usc.edu.
Rogers (United States) · USUniversity of Southern California · USUSC Norris Comprehensive Cancer Center · US

Funding

USC RESEARCH CENTER FOR LIVER DISEASES: PILOT PROGRAMSP30DK048522 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI OOKHTENS, MURAD · 1995 to 2020
$21.8M
MAPGen Knowledge Base (MAPGenKB) and Coordination CenterU01HL108634 · NHLBI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI CRANDALL, EDWARD DAVID, ZHOU, XIANGHONG JASMINE · 2011 to 2015
$5.3M
PULMONARY DEVELOPMENT-- MOLECULAR &CELLULAR ANALYSISR01HL056590 · NHLBI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI MINOO, PARVIZ MINOO · 1996 to 2012
$4.3M
Mechanisms of Lung Development and InjuryR01HL095349 · NHLBI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI MINOO, PARVIZ MINOO · 2009 to 2017
$3.6M
Mechanisms of beta-catenin signaling in alveolar epithelial cell differentiationR01HL112638 · NHLBI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI BOROK, ZEA, KAHN, MICHAEL · 2013 to 2016
$2.2M
Molecular programming of AEC differentiation: role of forkhead factorsR37HL062569 · NHLBI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI BOROK, ZEA · 2010 to 2014
$2.2M
Nanoparticle properties and alveolar epithelial barrier/transport functionsR01ES017034 · NIEHS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI CRANDALL, EDWARD DAVID · 2009 to 2013
$1.8M
Confocal Microscopy Imaging SystemS10RR022508 · NCRR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI OOKHTENS, MURAD · 2007 to 2007
$415k
NCRR NIH HHS S10 RR022508NHLBI NIH HHS R01HL056590NHLBI NIH HHS R01HL095349NHLBI NIH HHS R01 HL112638NHLBI NIH HHS R01HL112638NHLBI NIH HHS R37 HL062569NHLBI NIH HHS R37HL062569NHLBI NIH HHS U01HL108364NHLBI NIH HHS U01 HL108634NIDDK NIH HHS P30 DK048522NIEHS NIH HHS R01ES017034
6 · The paper itself

Abstract

Claudins are tight junction proteins that regulate paracellular ion permeability of epithelium and endothelium. Claudin 4 has been reported to function as a paracellular sodium barrier and is one of three major claudins expressed in lung alveolar epithelial cells (AEC). To directly assess the role of claudin 4 in regulation of alveolar epithelial barrier function and fluid homeostasis in vivo, we generated claudin 4 knockout (Cldn4 KO) mice. Unexpectedly, Cldn4 KO mice exhibited normal physiological phenotype although increased permeability to 5-carboxyfluorescein and decreased alveolar fluid clearance were noted. Cldn4 KO AEC monolayers exhibited unchanged ion permeability, higher solute permeability, and lower short-circuit current compared with monolayers from wild-type mice. Claudin 3 and 18 expression was similar between wild-type and Cldn4 KO alveolar epithelial type II cells. In response to either ventilator-induced lung injury or hyperoxia, claudin 4 expression was markedly upregulated in wild-type mice, whereas Cldn4 KO mice showed greater degrees of lung injury. RNA sequencing, in conjunction with differential expression and upstream analysis after ventilator-induced lung injury, suggested Egr1, Tnf, and Il1b as potential mediators of increased lung injury in Cldn4 KO mice. These results demonstrate that claudin 4 has little effect on normal lung physiology but may function to protect against acute lung injury.

Indexed as

Acute Lung InjuryAlveolar Epithelial CellsAnimalsCapillary PermeabilityCells, CulturedClaudin-4FemaleGene Knockout TechniquesGenetic Predisposition to DiseaseHyperoxiaLungMiceMice, 129 StrainMice, KnockoutPhenotypeTranscriptomeClaudin-4Cldn4 protein, mousealveolar epithelial barrieralveolar fluid clearancepermeabilityRNA sequencingventilator-induced lung injury

Identifiers

PMID25106430
PMCPMC4187039
OpenAlexW2151480919

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.