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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
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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.
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Overall design |
This study was designed to identify the gene expression profile of IL-4-dependent pulmonary vascular inflammation induced by hypoxia.
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Contributor(s) |
Cheadle C, Kegan K |
Citation missing |
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Submission date |
Sep 19, 2012 |
Last update date |
Jun 14, 2018 |
Contact name |
chris cheadle |
E-mail(s) |
[email protected]
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Phone |
4105505984
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Organization name |
JHU
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Department |
SOM
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Lab |
JHBMC Genomics Core
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Street address |
5200 Eastern Ave
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City |
baltimore |
State/province |
MD |
ZIP/Postal code |
21224 |
Country |
USA |
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Platforms (1) |
GPL6885 |
Illumina MouseRef-8 v2.0 expression beadchip |
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Samples (18)
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Relations |
BioProject |
PRJNA175515 |