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Vitamin D/VDR signaling inhibits LPS-induced IFNγ and IL-1β in Oral epithelia by regulating hypoxia-inducible factor-1α signaling pathway

机译:维生素D / VDR信号通过调节缺氧诱导因子1α信号通路抑制LPS诱导的口腔上皮中的IFNγ和IL-1β

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摘要

BackgroundOral lichen planus (OLP) is known as a chronic inflammatory disease. Our recent studies have suggested that vitamin D/vitamin D receptor (VDR) signaling exerts its protective effects on oral keratinocyte apoptosis by regulating microRNA-802 and p53-upregulated modulator of apoptosis (PUMA), but its roles in oral epithelial inflammatory responses in OLP are still unknown. Herein, we identify lipopolysaccharide (LPS) is able to enhance interferon gamma (IFNγ) and interleukin-1 beta (IL-1β) productions in human oral keratinocytes (HOKs) dependent on hypoxia-inducible factor-1α (HIF-1α).
机译:背景口腔扁平苔藓(OLP)被称为慢性炎症性疾病。我们最近的研究表明,维生素D /维生素D受体(VDR)信号传导通过调节microRNA-802和p53上调的凋亡调节剂(PUMA)对口腔角质形成细胞凋亡发挥保护作用,但在OLP的口腔上皮炎性反应中发挥作用仍然未知。在这里,我们确定脂多糖(LPS)能够增强依赖于缺氧诱导因子1α(HIF-1α)的人口腔角质形成细胞(HOKs)中的干扰素γ(IFNγ)和白介素1β(IL-1β)产生。

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