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作 者:杨艳琳 刘明[1] 邓樱[1] 郭艳[1] 张绪清[1] 向德栋[1] 蒋黎[1] 游忠岚[1] 伍艺 李茂仕[1] 毛青[1] Yang Yanlin;Liu Ming;Deng Ying;Guo Yah;Zhang Xuqing;Xiang Dedong;Jiang Li;You Zhonglan;Wu Yi;Li Maoshi;Mao Qing(Institute of Infectious Disease, Southwest Hospital, Army Medical University, Third Military Medical Universit;the Chongqing Key Laboratory for Research of Infectious Diseases, Chongqing 400038, Chin)
机构地区:[1]陆军军医大学(第三军医大学)西南医院全军感染病研究所感染病研究重庆市重点实验室,重庆400038
出 处:《中华实验和临床病毒学杂志》2018年第2期155-159,共5页Chinese Journal of Experimental and Clinical Virology
基 金:国家重点基础研究发展项目(973计划2013CB531501);国家传染病重点项目(2017ZX10202201)
摘 要:目的探究PegIFN治疗的CHB患者不同应答组用药前差异表达microRNAs,并分析其相应靶基因与HBsAg清除之间的关系。方法建立PegIFN治疗研究队列,运用高通量芯片获得PegIFN用药前不同应答组之间差异表达microRNAs,运用实时荧光定量PCR的方法进行验证,生物信息学分析差异microRNAs的靶基因及信号通路。结果芯片结果显示417条microRNAs在PegIFN的不同应答组之间差异表达,其中上调表达有342条,下调表达有75条,实时荧光定量PCR验证出miR-3960, miR-126-3p, miR-23 a-3p和miR-335-5p在HBsAg清除组下调。生物信息学分析,差异microRNAs的靶向基因相关的信号通路有:AMPK信号通路、NOD样受体信号通路、NF-kappa B信号通路、mTOR通路等。结论差异microRNAs可能通过调控免疫相关的基因表达,增强HBV清除相关的免疫应答,促进HBsAg清除。Objective To detect differentially expressed microRNAs in chronic hepatitis B ( CHB ) before being treated with pegylated interferon (PegIFN) and the relationship between their target genes and HBsAg loss. Methods Pretreatment differentially expressed microRNAs between different response groups were screened using high throughput microarrays and validated by quantitative reverse-transcription polymerase chain reaction ( RT-qPCR ). Bioinformatics analysis was performed to determine their target genes potential mechanistic roles. Results A total of 417 microRNA were differentially expressed between different response groups, among which 342 were up-regulated and 75 were down-regulated, miR-3960, miR-126-3p, miR-23 a-3p and miR-335-Sp were verified to be down-regulated by RT-qPCR result in HBsAg loss group. Bioinformatic analysis result show that the relevant pathways of microRNAs include AMPK signal pathway, NOD-like signal pathway, NF-kappa B signal pathway and mTOR signal pathway. Conclusions HBsAg loss is probably achieved as the result of genes expression regulated in association with immune response, further enhance the immune response of HBV elimination and acquire HBsAg loss.
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