Ning Shi

Jilin University, Yung-chi, Jilin Sheng, China

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Publications (2)3.58 Total impact

  • N Shi · X Y Zhang · C Y Dong · J L Hou · M L Zhang · Z H Guan · Z Y lI · M Duan ·
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    ABSTRACT: Rabies virus (RABV) is known to cause a fatal infection in many mammalian species, yet its pathogenesis remains poorly understood. This study was performed to analyze the microRNA (miRNA) expression profiles in RABV-infected primary neurons of mice. A total of 53 miRNAs were found to be differentially expressed in RABV-infected samples compared with mock samples in a time-dependent manner. Among them, the expression of ten miRNAs was validated by real-time RT-PCR. Potential target genes of differentially expressed miRNAs were predicted by TargetScan. Further bioinformatics analysis indicated that these predicted targets were overrepresented in neuronal function-related Gene Ontology (GO) terms and biological pathways. The results of this study suggest that RABV may cause neuronal dysfunction by regulating cellular miRNA expression. Keywords: rabies virus; microRNA; expression; microarray; neurons; mouse.
    Acta Virologica 06/2014; 58(2):120-7. DOI:10.4149/av_2014_02_120 · 1.28 Impact Factor
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    ABSTRACT: Influenza A virus is a cytolytic virus that induces apoptosis in numerous cell types, which contributes to cellular and organ dysfunction. MicroRNAs (miRNAs) represent a family of small noncoding RNAs controlling tanslation and transcription of many genes. Recent studies have revealed that miR-29c is involved in a variety of biological processes, including apoptosis. However, its role in influenza A virus infection is not well understood. Here, we report that miR-29c is involved in apoptosis induced by influenza A virus infection. We found that several apoptosis-associated miRNAs were stimulated in influenza A virus-infected A549 cells by miRNA array analysis. Within those, miR-29c was significantly up-regulated. In silico target prediction analysis revealed complementarity of miR-29c to the 3'-untranslated region (UTR) of BCL2L2 mRNA. Targeting of BCL2L2 3' UTR by miR-29c was determined by luciferase assay. Functional overexpression of miR-29c with miR-29c precursor inhibited BCL2L2 protein expression. Transfection of miR-29c inhibitor abolished both suppression of BCL2L2 protein expression and A549 cells apoptosis induced by influenza A virus. Moreover, BCL2L2 overexpression rescued A549 cell death induced by influenza A virus infection. These findings indicate that miR-29c-mediated BCL2L2 suppression is involved in influenza virus-induced cell death in A549 cells.
    Biochemical and Biophysical Research Communications 07/2012; 425(3):662-7. DOI:10.1016/j.bbrc.2012.07.114 · 2.30 Impact Factor

Publication Stats

10 Citations
3.58 Total Impact Points


  • 2012-2014
    • Jilin University
      • Department of Pathophysiology
      Yung-chi, Jilin Sheng, China