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Hierarchical control of the IL-13 signals by STAT6 and SOX11 in lung fibroblasts (MRC-5 cells)

ABSTRACT: To identify candidates for trans-acting factors for IL-13–induced genes in lung fibroblasts, we searched transcriptional factors among IL-13–inducible molecules in lung fibroblasts

ORGANISM(S): Homo sapiens

PROVIDER: GSE104936 | GEO | 2018/08/02

REPOSITORIES: GEO

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Hierarchical control of the IL-13 signals by STAT6 and SOX11 in lung fibroblasts (NHLF cells)

Project description:We sought to dissect SOX11-dependent and -independent genes in IL-13–inducible genes in primary human lung fibroblasts

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Hierarchical control of the IL-13 signals by STAT6 and SOX11 in lung fibroblasts (MRC-5 cells)

Project description:Hierarchical control of the IL-13 signals by STAT6 and SOX11 in lung fibroblasts (MRC-5 cells)

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Hierarchical control of the IL-13 signals by STAT6 and SOX11 in lung fibroblasts

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Hierarchical control of the IL-13 signals by STAT6 and SOX11 in lung fibroblasts (NHLF cells)

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Hierarchical control of interleukin 13 (IL-13) signals in lung fibroblasts by STAT6 and SOX11.

Project description:Interleukin (IL)-13 is a signature cytokine of type 2 inflammation important for the pathogenesis of various diseases, including allergic diseases. Signal transducer and activator of transcription (STAT) 6 is a critical transcriptional factor for the IL-13 signals; however, it remains unknown how expression of the IL-13-induced genes is differentiated by the transcriptional machineries. In this study, we identified IL-13-induced transcriptional factors in lung fibroblasts using DNA microarrays in which SOX11 was included. Knockdown of SOX11 down-regulated expression of periostin and CCL26, both of which are known to be downstream molecules of IL-13, whereas enforced expression of SOX11 together with IL-13 stimulation enhanced expression of periostin. Moreover, we found that in DNA microarrays combining IL-13 induction and SOX11 knockdown there exist both SOX11-dependent and -independent molecules in IL-13-inducible molecules. In the former, many inflammation-related and fibrosis-related molecules, including periostin and CCL26, are involved. These results suggest that SOX11 acts as a trans-acting transcriptional factor downstream of STAT6 and that in lung fibroblasts the IL-13 signals are hierarchically controlled by STAT6 and SOX11.

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TNF-alpha and IL-17 synergize to inhibit IL-13 bioactivity via IL-13Ra2 induction in human lung fibroblasts

Project description:IL-17 and TNF-alpha synergistically induce surface expression of IL-13Ra2 on primary lung fibroblasts, rendering them unresponsive to IL-13. Neutralizing antibodies to IL-13Ra2 restored IL-13-mediated signaling and transcriptome studies confirmed IL-13Ra2 is an IL-13 decoy receptor.

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Hierarchical control of the IL-13 signals by STAT6 and SOX11 in lung fibroblasts

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-08-02 | GSE104938 | GEO

IMR90 lung fibroblasts treated with IL-4 or IL-13

Project description:IL-4 and IL-13 are cytokines involved in type 2 immune responses involved in atopic asthma and other diseases. They have a partially overlapping set of cognate receptors whose roles are incompletely understood. Here we explore the effects of these cytokines on lung fibroblasts in order to assess the global similarities and contrasts in the genes whose expression their ligation modulates. IMR-90 lung fibroblast cells were cultured on matrigel or plastic and treated for 24 hours with IL-4 (10 ng/ml), IL-13 (10ng/ml), or TNFa (10 ng/ml) before harvest.

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Genome-wide analysis of gene expression for NHLF after treatment with 10 ng/ml of IL-13

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Myeloid cells or lung fibroblasts treated with IL-4 or IL-13

Project description:IL-4 and IL-13 are cytokines involved in type 2 immune responses involved in atopic asthma and other diseases. They have a partially overlapping set of cognate receptors whose roles are incompletely understood. Here we explore the effects of these cytokines on various cells related to human lung disease in order to assess the global similarities and contrasts in the genes whose expression their ligation modulates. Monocytes, monocyte-differentiated (6 days, then 24h rest) macrophages, or normal primary lung fibroblasts were cultured on matrigel and treated for 6 or 24 hours with IL-4 (10 ng/ml), IL-13 (10ng/ml), IL-10 (20 ng/ml), TGFb (10 ng/ml), or dexamethasone (0.5 uM) before harvest.

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