摘要
目的:检测hsa_circ_0023397和miR-106b在克罗恩病(Crohn's disease,CD)中的表达及其与自噬的关系,为CD的分子诊断和靶向治疗提供新思路。方法:在环状RNA芯片检测的基础上,收集活动期CD患者及健康体检者各40例,采用实时定量PCR检测肠黏膜组织中hsa_circ_0023397和miR-106b的表达情况,并用Western Blot检测自噬相关蛋白ATG16L1及LC3-Ⅱ/LC3-Ⅰ的表达情况。结果:与健康体检组相比,活动期CD患者肠黏膜组织中hsa_circ_0023397明显下降(P<0.01),而miR-106b显著升高(P<0.01)。Western Blot检测发现,活动期CD肠黏膜组织中ATG16L1及LC3-Ⅱ/LC3-Ⅰ比值均下降(P<0.05)。结论:活动期CD患者肠黏膜组织中可能存在着由于hsa_circ_0023397下调引起miR-106b过度表达,继而导致ATG16L1表达下调并降低CD患者自噬功能的新机制,有待进一步研究。
Objective:To investigate the expression of hsa_circ_0023397 and miR-106b in Crohn s disease(CD)and its relationship with autophagy and to provide new ideas for the molecular diagnosis and targeted therapy of CD.Methods:Based on the circRNA chip detection,hsa_circ_0023397 and miR-106b expresssion levels were analysed in 40 active CD patients and 40 health controls by the real-time quantitative reverse transcription-polymerase chain reaction(qRT-PCR).The expression of autophagy related protein ATG16L1 and LC3-II/LC3-I were assessed by Western Blot.Results:Compared with the healthy controls,the expression of hsa_circ_0023397 decreased significantly in active CD patients(P<0.01),whereas miR-106b expression level increased(P<0.01).Western Blot analysis revealed that the expression of ATG16L1 and LC3-II/LC3-I decreased in active CD(P<0.05).Conclusion:There may be a new mechanism that remains to be further studied for the overexpression of miR-106b due to the down-regulation of hsa_circ_0023397,leading to the down-regulation of ATG16L1 expression and reduction of the autophagy in the intestinal mucosal tissues of patients with active CD.
作者
沈朵
陈洪
李红霞
徐孝新
尹莹
SHEN Duo;CHEN Hong;LI Hong-xia;XU Xiao-xin;YIN Ying(School of Medicine,Southeast University,Nanjing 210009,China;Department of Digestive Disease,Zhongda Hospital,Southeast University,Nanjing 210009,China)
出处
《东南大学学报(医学版)》
CAS
2018年第1期22-27,共6页
Journal of Southeast University(Medical Science Edition)
基金
国家自然科学基金资助项目(81602432)
江苏省自然基金青年项目(BK20140652)