Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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RNAseq on lungs from WT vs claudin 4 KO mice that underwent ventilator-induced lung injury

ABSTRACT: WT mice and claudin 4 KO mice were exposed to ventilator-induced lung injury (VILI) for 2 hours. We found that in some Cldn4 KO mice, injury was similar to WT, while in others, injury was higher, as assessed by amount of protein leak into broncho-alveolar lavage fluid. We performed RNAseq to find which genes were responsible for higher injury in Cldn4 KO mice. WT mice and claudin 4 KO mice were exposed to ventilator-induced lung injury (VILI) for 2 hours. RNA were extracted from whole lungs and RNA sequencing was performed. The samples are (all in duplicates): WT no VILI, Cldn4 KO no VILI, WT VILI, Cldn4 KO VILI with similar injury to WT (Cldn4 KOlow), and Cldn4 KO VILI with higher injury than WT (Cldn4 KOhigh)

ORGANISM(S): Mus musculus

SUBMITTER: Zea Borok

PROVIDER: E-GEOD-50927 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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

Kage Hidenori H Flodby Per P Gao Danping D Kim Yong Ho YH Marconett Crystal N CN DeMaio Lucas L Kim Kwang-Jin KJ Crandall Edward D ED Borok Zea Z

American journal of physiology. Lung cellular and molecular physiology 20140808 7

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 physiolog ...[more]

PMID: 25106430

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Dataset Information

RNAseq on lungs from WT vs claudin 4 KO mice that underwent ventilator-induced lung injury

Publications

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

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