LncRNA-MSX2P1通过ROS/MAPK/自噬信号通路在银屑病中的调控作用

免疫功能紊乱是银屑病发病机制中的重要环节,T细胞及免疫活性分子介导的炎症反应发挥重要作用.LncRNA是一类从多层面调控基因表达的长链非编码RNA分子;MAPK信号通路在炎症反应中发挥重要作用;活性氧（ROS）能激活自噬，激活自噬的信号通路和MAPK密切相关.我们前期研究发现IL-22处理的HaCaT细胞及原代角质形成细胞lncRNA-MSX2P1高表达;干扰lncRNA-MSX2P1表达抑制炎症因子IL-23, NF-κB, TNF-α, IL-12β的表达,抑制增殖,促进凋亡;干扰lncRNA-MSX2P1表达可激活HaCaT细胞自噬.因此我们提出如下科学假说:通过干扰lncRNA-MSX2P1可激活ROS/MAPK/自噬信号通路,抑制炎症因子表达,从而影响银屑病的发生.本研究将采用慢病毒转染、流式细胞仪、WB、透射电镜等实验方法探讨lncRNA-MSX2P1在银屑病发病中的调控作用.

Immune dysfunction is an important part in the pathogenesis of psoriasis. Inflammatory response mediated by T cells and immune molecules plays important role in promoting the occurrence and development of psoriasis.The long noncoding RNA (lncRNA) are a class of long non-coding RNA , lncRNA can regulate gene expression at various levels.MAPK (mitogen-activated protein kinase) signaling pathway plays an important role in inflammation. The generation of reactive oxygen species (ROS) can induce autophagy and signaling pathway inducing autophagy is usually related to MAPK.In our previous study, the results showed that IL-22 treatment can promote the expression of lncRNA-MSX2P1 in HaCaT and primary cultured keratinocyte. lncRNA-MSX2P1 knockdown can suppress the expression of inflammatory factors,such as IL-23, NF-κB, TNF-αand IL-12β,suppress cell proliferation and promote cell apoptosis. lncRNA-MSX2P1 knockdown can activate cell autophagy in HaCaT. Based on our previous study, we present below scientific hypotheses: lncRNA-MSX2P1 knockdown can suppress the expression of inflammatory factors through activating ROS/MAPK/autophagy signaling pathway to influence occurrence of psoriasis. In this study, we will investigate the function of lncRNA-MSX2P1-ROS/MAPK/autophagy signaling axis in occurrence of psoriasis by Lentivirus transfection, flow cytometry ,western blot and transmission electron microscopy experimental method.