Hypoxia promotes the C5a-associated pathogenesis of rheumatoid arthritis via mi R-342-3p
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- 英文论文题名：Hypoxia promotes the C5a-associated pathogenesis of rheumatoid arthritis via mi R-342-3p
- 论文作者：Song Lijun ; Yi Lin ; Liu Juan ; Li Zhiqing ; Xia Meng ; Jiang Jinxia ; Wang Ye ; Cao xuetao ; Liu Shuxun
- 英文论文作者：Song Lijun ; Yi Lin ; Liu Juan ; Li Zhiqing ; Xia Meng ; Jiang Jinxia ; Wang Ye ; Cao xuetao ; Liu Shuxun ; Institute of Immunology and National Key Laboratory of Medical Immunology ; Second Military Medical University ; Institute of Immunology ; Zhejiang University School of Medicine ; National Key Laboratory of Medical Molecular Biology and Department of Immunology ; Chinese Academy of Medical Sciences
- 年：2016
- 作者机构：Institute of Immunology and National Key Laboratory of Medical Immunology,Second Military Medical University;Institute of Immunology,Zhejiang University School of Medicine;National Key Laboratory of Medical Molecular Biology and Department of Immunology,Chinese Academy of Medical Sciences;
- 英文论文关键词：Rheumatoid arthritis ; Hypoxia ; C5a ; miR-342-3p ; JAK/STAT
- 会议召开时间：2016-11-04
- 会议录名称：第十一届全国免疫学学术大会壁报交流集
- 英文会议录名称：Proceedings of 2016 CSI Congress on Immunology
- 语种：英文
- 分类号：R593.22
- 学会代码：IGMD
- 会议名称：第十一届全国免疫学学术大会
- 会议地点：中国安徽合肥
- 主办单位：中国免疫学会
- 学会名称：中国免疫学会
- 页数：1
- 文件大小：1023k
- 原文格式：D
- 会议级别：全国
摘要
Objective:Hypoxia-inducible micro RNAs(hi-mi R) are identified in hypoxia-associated physiological and pathogenic processes.Hypoxia is critical for the pathogenesis of several inflammatory diseases,particularly rheumatoid arthritis(RA).However,roles and underlying mechanisms of hi-mi R in autoimmune diseases remain poorly understood.Results:Considering that synovial dendritic cells(DCs) and C5a-associated inflammation are implicated in RA pathogenesis,here we investigated what hi-mi R regulated DCs to C5a-mediated inflammatory responses.Hypoxia promotes C5a-mediated responsiveness of DCs via upregulating C5 a R1 expressed on DCs from human monocytes by mi R-342-3p.Furthermore,mi R-342-3p targeted signal transducer and activator of transcription 5B(STAT5b),UBE2D3 and ubiquitin specific peptidase 13(USP13),thus maintaining C5 a R1 highly expressed on DCs via arresting STAT5/STAT6-mediated downregulation of C5 a R1 during monocytic differentiation into DCs.Blockade of mi R-342-3p abnormally increased in RA models significantly represses RA progression.Conclusion:So,our study identifies hypoxia-inducible mi R-342-3p as an important mediator for DCs and C5a-associated inflammatory pathogenesis in autoimmune diseases.
Objective:Hypoxia-inducible micro RNAs(hi-mi R) are identified in hypoxia-associated physiological and pathogenic processes.Hypoxia is critical for the pathogenesis of several inflammatory diseases,particularly rheumatoid arthritis(RA).However,roles and underlying mechanisms of hi-mi R in autoimmune diseases remain poorly understood.Results:Considering that synovial dendritic cells(DCs) and C5a-associated inflammation are implicated in RA pathogenesis,here we investigated what hi-mi R regulated DCs to C5a-mediated inflammatory responses.Hypoxia promotes C5a-mediated responsiveness of DCs via upregulating C5 a R1 expressed on DCs from human monocytes by mi R-342-3p.Furthermore,mi R-342-3p targeted signal transducer and activator of transcription 5B(STAT5b),UBE2D3 and ubiquitin specific peptidase 13(USP13),thus maintaining C5 a R1 highly expressed on DCs via arresting STAT5/STAT6-mediated downregulation of C5 a R1 during monocytic differentiation into DCs.Blockade of mi R-342-3p abnormally increased in RA models significantly represses RA progression.Conclusion:So,our study identifies hypoxia-inducible mi R-342-3p as an important mediator for DCs and C5a-associated inflammatory pathogenesis in autoimmune diseases.
Objective:Hypoxia-inducible micro RNAs(hi-mi R) are identified in hypoxia-associated physiological and pathogenic processes.Hypoxia is critical for the pathogenesis of several inflammatory diseases,particularly rheumatoid arthritis(RA).However,roles and underlying mechanisms of hi-mi R in autoimmune diseases remain poorly understood.Results:Considering that synovial dendritic cells(DCs) and C5a-associated inflammation are implicated in RA pathogenesis,here we investigated what hi-mi R regulated DCs to C5a-mediated inflammatory responses.Hypoxia promotes C5a-mediated responsiveness of DCs via upregulating C5 a R1 expressed on DCs from human monocytes by mi R-342-3p.Furthermore,mi R-342-3p targeted signal transducer and activator of transcription 5B(STAT5b),UBE2D3 and ubiquitin specific peptidase 13(USP13),thus maintaining C5 a R1 highly expressed on DCs via arresting STAT5/STAT6-mediated downregulation of C5 a R1 during monocytic differentiation into DCs.Blockade of mi R-342-3p abnormally increased in RA models significantly represses RA progression.Conclusion:So,our study identifies hypoxia-inducible mi R-342-3p as an important mediator for DCs and C5a-associated inflammatory pathogenesis in autoimmune diseases.
引文