MyD88 as a target of microRNA-203 in regulation of lipopolysaccharide or Bacille Calmette-Guerin induced inflammatory response of macrophage RAW264.7 cells

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• 作者：Jun Wei^a ; ^b ; Xuelan Huang^a ; Zhaobo Zhang^b ; Wei Jia^a ; ^b ; Zhijun Zhao^a ; ^b ; Ying Zhang^c ; Xiaoming Liu^d ; Guangxian Xu^a ; ^b ; ^{guangxianxu2004@yahoo.com.cn} ; ^{xgx205079@sina.com.cn}
• 关键词：miR-203 ; Myeloid differentiation factor 88 ; Lipopolysaccharide ; Bacille Calmette-Guerin (BCG) ; Inflammatory response
• 刊名：Molecular Immunology
• 出版年：2013
• 出版时间：October, 2013
• 年：2013
• 卷：55
• 期：3-4
• 页码：303-309
• 全文大小：828 K

文摘

MicroRNAs (miRNAs) have been demonstrated to play a pivotal role in the regulation of target gene expression at the post-transcriptional level. In order to better understand the role of microRNA-203 (miR-203) in the immunological regulation, the function of miR-203 was explored in the macrophage RAW264.7 cells against lipopolysaccharide (LPS) or Bacille Calmette-Guerin (BCG) stimulation. The results evidenced that myeloid differentiation factor 88 (MyD88) was a novel target of miR-203, miR-203 was capable of directly targeting the 3¡ä untranslated region (3¡äUTR) of MyD88 and post-transcriptionally down-regulating the expression of protein. In addition, an overexpression of miR-203 in RAW264.7 cells was correlated with repressions of MyD88, as well as its downstream signaling of NF-¦ÊB (NF-¦ÊB1), TNF-¦Á and IL-6. These results suggest that miR-203 may be an important regulator in macrophages against LPS or mycobacteria infection, which may through a mechanism of negatively regulating MyD88-dependent Toll-like receptors signaling pathway.