IncRNAJPX 通过mA-YTHDC2轴上调细胞质p21蛋白促进RA-FLS增殖

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关键词：lncRNAJPX；类风湿关节炎成纤维细胞样滑膜细胞（RA-FLS）； p21 ; N6 甲基腺苷 （m6A） ；含YTH结构域蛋白2（YTHDC2）

中图分类号：R593.22

文献标志码：A

ABSTRACT：The aimof the present study was to reveal the underlying molecular mechanism by which lncRNA JPX regulated theactivityof rheumatoid arthritisfibroblast-likesynoviocytes （RA-FLS）.Thereverse transcription-quantitativereal-time polymerase chain reaction（RT-qPCR），Western blot，methylated RNA immunoprecipitation （MeRIP） assay，luciferase reporter assy，RNA immunoprecipitation（RIP）assay，protein stabilityassay，andin uitro functional experiments were performed to explore the role and molecular mechanismof JPX in regulating RA-FLS activation. The results showed that JPX increased the N6 -methyladenosine （ in6A ）modification in ，which increased its interaction with YTHDC2 toupregulate theexpresionof p21 protein inRA-FLS.Meanwhile，JPX further increased theenrichment of p21 protein inthecytoplasmof RA-FLS and subsequentlypromoted their proliferation. In summary，JPX canregulate RA-FLS proliferation through an m6 A-YTHDC2-p21 axis and the distribution of p21 protein in cells. JPX might be a novel target for RA diagnosis and treatment.

KEY WORDS： lncRNA JPX； rheumatoid arthritis fibroblast-like synoviocytes （RA-FLS）； p21； N6 -methyladenosine（m6A） ；YTH domain containing 2（YTHDC2）

类风湿关节炎（rheumatoidarthritis，RA）是一种以慢性炎症和滑膜关节破坏为特征的自身免疫性疾病，其病理改变主要包括滑膜增生、滑膜炎症、血管翳形成、骨质破坏等，最终导致关节损伤、畸形和致残[1-2]。（剩余14401字）