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MicroRNA expression data from IL13-induced allergic airway inflammation of mice lungs

ABSTRACT: Epigenetic changes have been implicated in pathogenesis of asthma. We sought to determine if IL13, a key cytokine in airway inflammation and remodeling, induced miRNAs expression changes in the airways in conjunction with its transcriptional gene regulation. For our studies, we used a well-characterized transgenic mouse model of allergic airway inflammation induced by IL13. In this model, IL13 is conditionally overexpressed in the mouse lung when treated with doxycycline. Upon IL13 induction, these mice showed inflammatory cell infiltration, pronounced emphysema, increased pulmonary compliance, lung volume enlargement, mucus metaplasia, and increased expression of matrix metalloproteinases and cathepsins in the lung. The CC10-rtTA-IL13 transgenic (TG) and wildtype (WT) mice were treated with doxycycline for seven days. Mice were euthanized and the left upper lobes from all mice were removed for RNA extraction using the TRIzol method.

ORGANISM(S): Mus musculus

SUBMITTER: Aik Ooi

PROVIDER: E-GEOD-35980 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gene expression data from IL13-induced allergic airway inflammation of mice lungs

Project description:Asthma is a common chronic inflammatory airway condition with a strong genetic and inheritability component, as siblings and first-degree relatives of those with the disease are often affected. For our studies, we used a well-characterized transgenic mouse model of allergic airway inflammation induced by IL13. In this model, IL13 is conditionally overexpressed in the mouse lung when treated with doxycycline. Upon IL13 induction, these mice showed inflammatory cell infiltration, pronounced emphysema, increased pulmonary compliance, lung volume enlargement, mucus metaplasia, and increased expression of matrix metalloproteinases and cathepsins in the lung. We performed gene expression microarray to examine the changes in gene expression during IL13-induced allergic airway inflammation. The CC10-rtTA-IL13 transgenic (TG) and wildtype (WT) mice were treated with doxycycline for seven days. Mice were euthanized and the left upper lobes from all mice were removed for RNA extraction using the TRIzol method.

2012-02-23 | E-GEOD-35979 | biostudies-arrayexpress

Methylated DNA immunoprecipitation (MeDIP) microarray data from IL13-induced allergic airway inflammation of mouse lungs

Project description:Epigenetic changes have been implicated in pathogenesis of asthma. We sought to determine if IL13, a key cytokine in airway inflammation and remodeling, induced epigenetic DNA methylation changes in the airways in conjunction with its transcriptional gene regulation. For our studies, we used a well-characterized transgenic mouse model of allergic airway inflammation induced by IL13. In this model, IL13 is conditionally overexpressed in the mouse lung when treated with doxycycline. Upon IL13 induction, these mice showed inflammatory cell infiltration, pronounced emphysema, increased pulmonary compliance, lung volume enlargement, mucus metaplasia, and increased expression of matrix metalloproteinases and cathepsins in the lung. We performed MeDIP microarray to examine the changes in DNA promoter methylation during IL13-induced allergic airway inflammation. The CC10-rtTA-IL13 transgenic (TG) and wildtype (WT) mice were treated with doxycycline for seven days. Mice were euthanized and the left lower lobes from all mice were removed for DNA extraction followed by MeDIP array analysis.

2012-04-06 | E-GEOD-37079 | biostudies-arrayexpress

MicroRNA expression data from IL13-induced allergic airway inflammation of mice lungs

2012-02-23 | GSE35980 | GEO

Gene expression data from IL13-induced allergic airway inflammation of mice lungs

2012-02-23 | GSE35979 | GEO

Methylated DNA immunoprecipitation (MeDIP) microarray data from IL13-induced allergic airway inflammation of mouse lungs

2012-04-07 | GSE37079 | GEO

MicroRNA profiling of mouse samples untreated and doxycycline treated CC10-IL13 animals

Project description:The aim of this experiment is to determine microRNAs that are diffferentially regulated in allergic airway inflammation. MicroRNA expression profile between untreated and doxycycline treated CC10-IL13 bitransgenic mice

2009-04-15 | E-MEXP-1992 | biostudies-arrayexpress

Expression and MeDIP microarray data from IL13-induced allergic airway inflammation of mice lungs

Project description:This SuperSeries is composed of the following subset Series: GSE35979: Gene expression data from IL13-induced allergic airway inflammation of mice lungs GSE35980: MicroRNA expression data from IL13-induced allergic airway inflammation of mice lungs GSE37079: Methylated DNA immunoprecipitation (MeDIP) microarray data from IL13-induced allergic airway inflammation of mouse lungs Refer to individual Series

2012-04-06 | E-GEOD-37085 | biostudies-arrayexpress

Analysis of miRNA expression in lung (CC10) VEGF transgenic mice and their wild type litters

Project description:Vascular Endothelial Growth Factor (VEGF) is a critical regulator of pulmonary Th2 inflammation but the underlying mechanism and the roles of miRNAs in this process have not been defined. We analyzed the effect of VEGF on lung microRNAs by microarray analysis and validated the findings by Taqman qRT-PCR. We compared the levels of microRNAs in the lungs of transgenic mice with their wild type litters after overexpression of VEGF from a lung epithelium-restricted transgene. VEGF was overexpressed in the lung epithelium of CC10-rtTA-VEGF transgenic mice by adding Doxycycline to their drinking water for 7-10 days. RNA from the lungs of VEGF transgenic mice and their wild type litters were extracted and analyzed by microarray. The expression levels of microRNAs that were significanly altered were validated in another group of mice.

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Expression data from human airway epithelia exposed to IL13

Project description:IL13 exposure results in a distinct gene expression profile in human airway epithelia. We investigated whether this expression profile can be used to identify compounds able to block goblet cell metaplasia We used microarrays to determine transcriptional changes in cultures of primary human airway epithelia grown at the air-liquid interface after exposure to 20 ng/mL recombinant human IL13

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IL13 and CCL2 drive disease in an inflammatory subset of Scleroderma [IL13]

Project description:Scleroderma is a lethal and currently irreversible autoimmune disease characterized by widespread tissue fibrosis and vasculopathy. Using cross-species comparative gene expression profiling we show that murine sclerodematous graft-versus-host disease (sclGVHD) approximates an “inflammatory” subset of human scleroderma and that both diseases demonstrate activation of the IL13 cytokine pathway. We report that both host myeloid cells expressing type I and II activated macrophage markers and graft T-cells produce IL13 and that host mice deficient in either IL13 or IL4Ra, an IL13 signal transducer, are protected from disease. This signaling pathway converges on a single gene, CCL2, which is coordinately upregulated in sclGVHD, in the human inflammatory scleroderma subset and in IL13 treated human dermal fibroblasts. Accordingly, treatment with antibodies to CCL2, and its murine homolog CCL12, prevent sclGVHD. Lastly, we provide evidence that IL13 pathway activation in early scleroderma patients correlates with modified Rodnan skin scores (mRSS). These data indicate that an inflammatory subset of scleroderma is driven by IL13 and may benefit from IL13 or CCL2 blockade.

2011-06-30 | GSE24403 | GEO

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