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Regulation of pro-inflammatory cytokines TNFα and IL24 by microRNA-203 in primary keratinocytes

机译：microRNA-203在原代角质形成细胞中对促炎细胞因子TNFα和IL24的调节

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Cutaneous homeostasis and innate immunity is procured by a complex circuitry of intercellular cytokine signaling. MicroRNAs are important posttranscriptional regulators of keratinocyte gene expression and assist in modulating the fine balance between cell proliferation and differentiation in skin. A characteristic microRNA profile in inflammatory skin suggests putative functions of microRNAs in perturbed cytokine production and signaling during chronic inflammatory skin conditions such as psoriasis. It remains unclear, however, why certain microRNAs are aberrantly expressed during skin inflammation and if they serve pro- and/or anti-inflammatory functions. In this report, we focus on cytokine regulation by microRNA-203 (miR-203), which is highly abundant in keratinocytes and upregulated in psoriatic lesions. By screening a panel of cytokines that are upregulated in psoriatic skin for regulation by miR-203, we identify the genes encoding the pro-inflammatory cytokines TNFα and IL24 as direct targets of miR-203. Studies of miR-203 overexpression, inhibition, and mutagenesis validate posttranscriptional regulation of TNFα and IL24 by miR-203 in cell lines and primary keratinocytes. Our findings suggest that miR-203 serves to fine-tune cytokine signaling and may dampen skin immune responses by repressing key pro-inflammatory cytokines.
机译：皮肤稳态和先天免疫是由细胞间细胞因子信号传导的复杂电路实现的。 MicroRNA是角质形成细胞基因表达的重要转录后调节剂，有助于调节皮肤细胞增殖与分化之间的精细平衡。炎性皮肤中的特征性microRNA谱表明，在慢性炎性皮肤病（如牛皮癣）期间，microRNA可能在扰动的细胞因子产生和信号传导中具有假定的功能。然而，尚不清楚为什么某些microRNA在皮肤发炎期间异常表达，以及它们是否具有促炎和/或抗炎功能。在本报告中，我们着重于通过microRNA-203（miR-203）调控细胞因子，microRNA-203在角质形成细胞中高度丰富，在银屑病皮损中上调。通过筛选银屑病皮肤中上调的一组细胞因子以通过miR-203进行调节，我们确定了编码促炎性细胞因子TNFα和IL24的基因作为miR-203的直接靶标。 miR-203过表达，抑制和诱变的研究证实了miR-203在细胞系和原代角质形成细胞中对TNFα和IL24的转录后调控。我们的发现表明，miR-203可微调细胞因子信号传导，并可能通过抑制关键的促炎性细胞因子来抑制皮肤免疫反应。

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