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Series GSE40999 Query DataSets for GSE40999
Status Public on Sep 19, 2013
Title Th2 cytokine IL-4 is critical in initiating pulmonary vascular inflammation under hypoxic conditions and induces pulmonary vascular endothelial cell activation.
Organism Mus musculus
Experiment type Expression profiling by array
Summary IL-4-mediated pro-inflammatory vascular responses have been implicated in the pathogenesis of chronic cardiopulmonary diseases.
Our results show that hypoxia-induced collagen synthesis and early recruitment of inflammatory cells are significantly less in the lungs of IL-4 knockout (KO) mice than in those of wild-type mice. In addition, we found that IL-4 significantly increased pro-inflammatory genes in primary pulmonary microvascular endothelial cells.
 
Overall design This study was designed to identify the gene expression profile of IL-4-dependent pulmonary vascular inflammation induced by hypoxia.
 
Contributor(s) Cheadle C, Kegan K
Citation missing Has this study been published? Please login to update or notify GEO.
Submission date Sep 19, 2012
Last update date Jun 14, 2018
Contact name chris cheadle
E-mail(s) [email protected]
Phone 4105505984
Organization name JHU
Department SOM
Lab JHBMC Genomics Core
Street address 5200 Eastern Ave
City baltimore
State/province MD
ZIP/Postal code 21224
Country USA
 
Platforms (1)
GPL6885 Illumina MouseRef-8 v2.0 expression beadchip
Samples (18)
GSM1006633 RJ7-1
GSM1006634 RJ7-2
GSM1006635 RJ7-3
Relations
BioProject PRJNA175515

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE40999.txt.gz 132 b (ftp)(http) TXT
GSE40999_RAW.tar 3.1 Mb (http)(custom) TAR
GSE40999_non-normalized.txt.gz 2.1 Mb (ftp)(http) TXT
Processed data included within Sample table

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