MiR-196a regulates heme oxygenase-1 by silencing Bach1 in the neonatal mouse lung

DOI Web Site PubMed 被引用文献1件 参考文献45件
  • Hayato Go
    Department of Neonatology, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania;
  • Ping La
    Department of Neonatology, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania;
  • Fumihiko Namba
    Department of Neonatology, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania;
  • Masato Ito
    Department of Pediatrics, Saitama Medical Center, Saitama, Japan
  • Guang Yang
    Department of Neonatology, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania;
  • Andrey Brydun
    Department of Biochemistry, Tohoku University Graduate School of Medicine, Sendai, Japan;
  • Kazuhiko Igarashi
    Department of Biochemistry, Tohoku University Graduate School of Medicine, Sendai, Japan;
  • Phyllis A. Dennery
    Department of Neonatology, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania;

書誌事項

公開日
2016-08-01
資源種別
journal article
DOI
  • 10.1152/ajplung.00428.2015
公開者
American Physiological Society

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説明

<jats:p> In the lung, heme oxygenase-1 (HO-1) is developmentally regulated, with its highest expression in the first days of life. In addition, neonatal mice have limited HO-1 induction in hyperoxia compared with adults. However, few reports have addressed the functional effect of microRNAs (miRNAs) in the regulation of HO-1 in vivo. The aims of the present study were to characterize changes in lung miRNA expression during postnatal development and in response to hyperoxic exposure, and to identify miRNAs that target lung HO-1 gene expression. Neonatal (<12 h old) and adult (2 mo old) mice were exposed to room air or hyperoxia (95% oxygen) for 72 h. TaqMan low-density array rodent miRNA assays were used to calculate miRNA expression changes between control and hyperoxia groups in neonatal and adult lungs. In neonates, we identified miR-196a, which binds to the 3′-untranslated region of the transcriptional repressor BTB and CNC homology 1 (Bach1) and regulates its expression, and subsequently leads to higher levels of lung HO-1 mRNA compared with levels in adults. Despite the increase at baseline, miR-196a was degraded in hyperoxia resulting in limited HO-1 induction in neonatal mice lungs. Furthermore, the developmental differences in lung HO-1 gene expression can be explained in part by the variation in miRNA-196a and its effect on Bach1. This report is the first to show developmental differences in lung miR-196a and its effect on Bach1 and HO-1 expression at baseline and in hyperoxia. </jats:p>

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