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中国循证儿科杂志

中国循证儿科杂志 ›› 2019, Vol. 14 ›› Issue (1): 49-53.

• 论著 • 上一篇    下一篇

长链非编码RNA LINC01503在哮喘患儿中的表达及作用的病例对照研究

夏莉1,3刘丽娟1,3王香1孙立成1付劲蓉1 韩晓1钱莉玲1周玉峰1,2   

  1. 1 复旦大学附属儿科医院和生物医学研究院 上海，201102； 2 卫生部新生儿疾病重点实验室 上海，201102；3 共同第一作者
  • 收稿日期:2018-12-28 修回日期:2019-02-25 出版日期:2019-02-25 发布日期:2019-02-25
  • 通讯作者: 周玉峰

The preliminary study of the expression of long non-coding RNA LINC01503 in children asthmatic patients and its function

XIA Li 1,3, LIU Li-juan1,3,WANG Xiang1, SUN Li-cheng1, FU Jin-rong1, HAN Xiao1, QIAN Li-ling1,ZHOU Yu-feng 1,2,3   

  1. 1 Children's Hospital and Institutes of Biomedical Sciences of Fudan University, Shanghai 201102,China; 2 Key Laboratory of Neonatal Diseases, Ministry of Health, Shanghai 201102, China; 3 Co-first author
  • Received:2018-12-28 Revised:2019-02-25 Online:2019-02-25 Published:2019-02-25
  • Contact: ZHOU Yu-feng

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摘要： 目的研究长链非编码RNA LINC01503在哮喘患儿中的表达及在巨噬细胞极化中的调控作用，为完善哮喘发病机制及发现新的防治靶点提供实验依据。方法纳入2017年8月26日至2018年1月11日复旦大学附属儿科医院（我院）呼吸科门诊确诊的哮喘患儿（哮喘组）及我院健康体检儿童（健康对照组），分离2组外周血中的单个核细胞，采用RT-qPCR检测LINC01503在两组中的表达；LPS 与IL-4 分别诱导巨噬细胞向M1及M2方向极化，采用RT-qPCR检测LINC01503的动态变化；脂质体转染siRNA敲低 LINC01503表达，采用RT-qPCR 及Western blot 检测LINC01503对巨噬细胞极化的影响。结果哮喘组28例，健康对照组46例。与健康对照组相比， LINC01503在哮喘组中的表达显著升高。LINC01503 在M1巨噬细胞中明显下调，而在M2巨噬细胞中明显上调。siRNA敲低实验发现，LINC01503 促进M1巨噬细胞的极化，上调M1 标志基因如IL-6、TNF-α和CXCL10等的表达； LINC01503 抑制M2巨噬细胞的极化，下调M2 标志基因如CD206和CD209的表达。Western blot 发现LINC01503 主要通过促进细胞外调节蛋白激酶（ERK）的磷酸化而影响巨噬细胞极化。结论LINC01503在哮喘患儿中高表达，通过负反馈调控巨噬细胞的活化，有望成为哮喘治疗的新靶点。

Abstract: ObjectiveTo explore the potential role of LINC01503 in the regulation of macrophage polarization and its function in the pathology of children asthma to achieve a better understanding of the pathology of asthma and find new strategies for asthma treatment. MethodsBlood was collected from asthmatic patients and healthy controls from August 26, 2017 to January 11, 2018 at Children's Hospital of Fudan University. PBMCs were separated from blood by gradient centrifuge. RT-qPCR was used for the detection of the expression of LINC01503 in PBMCs. LPS and IL-4 were used for the inducing of M1 and M2 polarization of macrophage separately. siRNA was used for knocking down LINC01503. RT-qPCR and Western blot were used for the detection of the effect of LINC01503 on the regulation of macrophage polarization. ResultsWe enrolled 28 patients of asthma and 46 healthy controls. Comparing with healthy controls，the expression of LINC01503 was significantly enhanced in asthmatic patients. LINC01503 was up-regulated in M2 macrophage but down-regulated in M1 macrophage. LINC01503 inhibited the M2 macrophage polarization indicated as the down regulation of CD206 and CD209. On the opposite, LINC01503 promoted the M1 macrophage polarization indicated as the up regulation of the expression of inflammatory mediators such as IL-6, TNF-α and CXCL10 through enhancing the phosphorylation of ERK. ConclusionLINC01503 was up-regulated in the asthmatic patients and it regulated macrophage polarization through a negative feedback loop.