MiR-122 modulates type I interferon expression through blocking suppressor of cytokine signaling 1

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• 作者：Aimei Li^a ; ^b ; ¹ ; ^{liaimeiandamy@126.com} ; Wuqi Song^a ; ^b ; ^c ; ¹ ; ^{songwuqi@yahoo.com.cn} ; Jun Qian^a ; ^b ; ¹ ; ^{junqian1978@163.com} ; Yujun Li^a ; ^b ; ^c ; ^{Li_yujun@126.com} ; Junming He^a ; ^b ; ^{hejunming137@163.com} ; Qingmeng Zhang^a ; ^b ; ^{qmzhang@yahoo.cn} ; Wenhui Li^a ; ^b ; ^{429413198@qq.com} ; Aixia Zhai^a ; ^b ; ^{zhaiaixia@126.com} ; Wenping Kao^a ; ^b ; ^{hm_519@163.com} ; Yunlong Hu^a ; ^b ; ^{jackyhu@126.com} ; Hui Li^a ; ^b ; ^{Lihui9406@sina.com} ; Jing Wu^a ; ^b ; ^{wujing_1227@126.com} ; Hong Ling^a ; ^b ; ^{profling2003@yahoo.com} ; Zhaohua Zhong^a ; ^b ; ^{zhongzh@hrbmu.edu.cn} ; Fengmin Zhang^a ; ^b ; ^c ; ^{fengminzhang@yahoo.com.cn}
• 关键词：MiRNA ; MiR-122 ; Suppressor of cytokine signaling 1 ; Type I interferon ; Hepatocytes
• 刊名：The International Journal of Biochemistry and Cell Biology
• 出版年：2013
• 出版时间：April, 2013
• 年：2013
• 卷：45
• 期：4
• 页码：858-865
• 全文大小：1326 K

文摘

MiR-122 is a liver-speci?c miRNA. Recent studies demonstrated that the interferon (IFN) therapy efficacy is poor in the hepatitis C virus (HCV)-infected patients with lower miR-122 abundance in the livers. The hepatocarcinoma patients also have low miR-122 levels in their livers. We previously found that the IFN expression was reduced when miR-122 was knocked down in human oligodendrocytes. The mechanism is unclear. In this study, the miR-122-abundant cell Huh7 was used to explore the regulatory mechanism of miR-122 on type I IFN expression. We found that miR-122 significantly increased the type I IFN expression in Huh7 cells, while knocking down miR-122 decreased the type I IFN expression. By screening potential miR-122 targets among the negative regulators in IFN signaling pathways, we found that there were putative miR-122 targets in the suppressor of cytokine signaling 1 (SOCS1) mRNA. Over-expressing miR-122 decreased the SOCS1 expression by 50.55 % in Huh7 cells, while knocking down miR-122 increased SOCS1 expression by 62.56 % . Using a green fluorescence protein (EGFP) fused SOCS1-expressing plasmid, the SOCS1-EGFP fluorescence intensity and protein were lower in miR-122 mimic-treated cells than those in mock-miRNA-treated cells, while miR-122 knockdown significantly increased the SOCS1-EGFP fluorescence intensity and protein expression. Mutations in the nt359-nt375 region abandoned the impact of miR-122 on SOCS1-EGFP expression. Taken together, SOCS1 is a target of miR-122. MiR-122 can regulate the type I IFN expression through modulating the SOCS1 expression.