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Although microRNAs (miRNAs) have been shown to control the IFN response in immune cells in LN, the role of miRNAs in resident renal cells remains unclear. We undertook this study to investigate the role of microRNA\u2010130b (miR\u2010130b) in the IFN pathway in renal cells as well as its therapeutic effect in LN.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Kidney tissues from patients and (NZB \u00d7 NZW)F1 lupus\u2010prone mice were collected for detecting miR\u2010130b levels. Primary renal mesangial cells (RMCs) were used to determine the role of miR\u2010130b in the IFN pathway. We overexpressed miR\u2010130b by administering miR\u2010130b agomir in a mouse model of IFN\u03b1\u2010accelerated LN to test its therapeutic efficacy.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Down\u2010regulated miR\u2010130b expression was observed in kidney tissues from patients and lupus\u2010prone mice. Further analysis showed that underexpression of miR\u2010130b correlated negatively with abnormal activation of the IFN response in LN patients. In vitro, overexpressing miR\u2010130b suppressed signaling downstream from the type I IFN pathway in RMCs by targeting IFN regulatory factor 1 (IRF\u20101). The opposite effect was observed when endogenous miR\u2010130b expression was inhibited. The inverse correlation between\n                      <jats:italic>IRF1<\/jats:italic>\n                      and miR\u2010130b levels was detected in renal biopsy samples from LN patients. More importantly, in vivo administration of miR\u2010130b agomir reduced IFN\u03b1\u2010accelerated progression of LN, with decreased proteinuria, lower levels of immune complex deposition, and lack of glomerular lesions.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>MicroRNA\u2010130b is a novel negative regulator of the type I IFN pathway in renal cells. Overexpression of miR\u2010130b in vivo ameliorates IFN\u03b1\u2010accelerated LN, providing potential novel strategies for therapeutic intervention in LN.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/art.39725","type":"journal-article","created":{"date-parts":[[2016,4,25]],"date-time":"2016-04-25T20:22:49Z","timestamp":1461615769000},"page":"2232-2243","source":"Crossref","is-referenced-by-count":57,"title":["MicroRNA\u2010130b Ameliorates Murine Lupus Nephritis Through Targeting the Type I Interferon Pathway on Renal Mesangial Cells"],"prefix":"10.1002","volume":"68","author":[{"given":"Xiao","family":"Han","sequence":"first","affiliation":[{"name":"Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, and Shanghai Jiao Tong University School of Medicine Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yan","family":"Wang","sequence":"additional","affiliation":[{"name":"Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, and Shanghai Jiao Tong University School of Medicine Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaoyan","family":"Zhang","sequence":"additional","affiliation":[{"name":"Shanghai Institute of Rheumatology, Renji Hospital, and Shanghai Jiao Tong University School of Medicine Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuting","family":"Qin","sequence":"additional","affiliation":[{"name":"Shanghai Institute of Rheumatology, Renji Hospital, and Shanghai Jiao Tong University School of Medicine Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bo","family":"Qu","sequence":"additional","affiliation":[{"name":"Shanghai Institute of Rheumatology, Renji Hospital, and Shanghai Jiao Tong University School of Medicine Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lingling","family":"Wu","sequence":"additional","affiliation":[{"name":"Shanghai Institute of Rheumatology, Renji Hospital, and Shanghai Jiao Tong University School of Medicine Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jianyang","family":"Ma","sequence":"additional","affiliation":[{"name":"Shanghai Institute of Rheumatology, Renji Hospital, and Shanghai Jiao Tong University School of Medicine Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhenyuan","family":"Zhou","sequence":"additional","affiliation":[{"name":"Shanghai Institute of Rheumatology, Renji Hospital, and Shanghai Jiao Tong University School of Medicine Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jie","family":"Qian","sequence":"additional","affiliation":[{"name":"Shanghai Institute of Rheumatology, Renji Hospital, and Shanghai Jiao Tong University School of Medicine Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Min","family":"Dai","sequence":"additional","affiliation":[{"name":"Shanghai Institute of Rheumatology, Renji Hospital, and Shanghai Jiao Tong University School of Medicine Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuanjia","family":"Tang","sequence":"additional","affiliation":[{"name":"Shanghai Institute of Rheumatology, Renji Hospital, and Shanghai Jiao Tong University School of Medicine Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Edward K. 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