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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE104938 | GEO | 2018/08/02

REPOSITORIES: GEO

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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.

| S-EPMC6153291 | biostudies-literature

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

2018-08-02 | GSE104937 | GEO

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

Project description: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

2018-08-02 | GSE104936 | GEO

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

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

| PRJNA414187 | ENA

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

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

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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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IL-13 induces YY1 through the AKT pathway in lung fibroblasts.

Project description:A key feature of lung fibrosis is the accumulation of myofibroblasts. Interleukin 13 (IL-13) is a pro-fibrotic mediator that directly and indirectly influences the activation of myofibroblasts. Transforming growth factor beta (TGF-β) promotes the differentiation of fibroblasts into myofibroblasts, and can be regulated by IL-13. However, IL-13's downstream signaling pathways are not completely understood. We previously reported that the transcription factor Yin Yang 1 (YY1) is upregulated in fibroblasts treated with TGF-β and in the lungs of mice and patients with pulmonary fibrosis. Moreover, YY1 directly regulates collagen and alpha smooth muscle actin (α-SMA) expression in fibroblasts. However, it is not known if IL-13 regulates fibroblast activation through YY1 expression. We hypothesize that IL-13 up-regulates YY1 expression through regulation of AKT activation, leading to fibroblast activation. In this study we found that YY1 was upregulated by IL-13 in lung fibroblasts in a dose- and time-dependent manner, resulting in increased α-SMA. Conversely, knockdown of YY1 blocked IL-13-induced α-SMA expression in fibroblasts. Furthermore, AKT phosphorylation was increased in fibroblasts treated with IL-13, and AKT overexpression upregulated YY1, whereas blockade of AKT phosphorylation suppressed the induction of YY1 by IL-13 in vitro. In vivo YY1 was upregulated in fibrotic lungs from CC10-IL-13 transgenic mice compared to that from wild-type littermates, which was associated with increased AKT phosphorylation. Taken together, these findings demonstrate that IL-13 is a potent stimulator and activator of fibroblasts, at least in part, through AKT-mediated YY1 activation.

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Primary lung fibroblasts respond to IL-33, IL-13, and IL-17a and secrete factors that activate macrophages

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

2024-09-03 | GSE226344 | 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.

2013-12-31 | GSE47542 | GEO

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

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