IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v3y2012i1d10.1038_ncomms1770.html
   My bibliography  Save this article

miR-484 regulates mitochondrial network through targeting Fis1

Author

Listed:
  • Kun Wang

    (State Key Laboratory of Biomembrane and Membrane Biotechnology, Institute of Zoology, Chinese Academy of Sciences)

  • Bo Long

    (State Key Laboratory of Biomembrane and Membrane Biotechnology, Institute of Zoology, Chinese Academy of Sciences)

  • Jian-Qin Jiao

    (State Key Laboratory of Biomembrane and Membrane Biotechnology, Institute of Zoology, Chinese Academy of Sciences)

  • Jian-Xun Wang

    (State Key Laboratory of Biomembrane and Membrane Biotechnology, Institute of Zoology, Chinese Academy of Sciences)

  • Jin-Ping Liu

    (State Key Laboratory of Biomembrane and Membrane Biotechnology, Institute of Zoology, Chinese Academy of Sciences)

  • Qian Li

    (State Key Laboratory of Biomembrane and Membrane Biotechnology, Institute of Zoology, Chinese Academy of Sciences)

  • Pei-Feng Li

    (State Key Laboratory of Biomembrane and Membrane Biotechnology, Institute of Zoology, Chinese Academy of Sciences)

Abstract

Mitochondria constantly undergo fusion and fission, two necessary processes for the maintenance of organelle fidelity. The abnormal mitochondrial fission participates in the pathogenesis of many diseases, but its regulation remains poorly understood. Here we show that miR-484 can suppress translation of mitochondrial fission protein Fis1, and inhibit Fis1-mediated fission and apoptosis in cardiomyocytes and in the adrenocortical cancer cells. We demonstrate that Fis1 is necessary for mitochondrial fission and apoptosis, and is upregulated during anoxia, whereas miR-484 is downregulated. miR-484 is able to attenuate Fis1 upregulation and mitochondrial fission, by binding to the amino acid coding sequence of Fis1 and inhibiting its translation. In exploring the underlying mechanism of miR-484 downregulation upon apoptosis, we observe that Foxo3a transactivates miR-484 expression. Foxo3a transgenic or knockout mice exhibit, respectively, a high or low level of miR-484 and a reduced or enhanced mitochondrial fission, apoptosis and myocardial infarction. Our data reveal a model of mitochondrial fission regulation by a microRNA.

Suggested Citation

  • Kun Wang & Bo Long & Jian-Qin Jiao & Jian-Xun Wang & Jin-Ping Liu & Qian Li & Pei-Feng Li, 2012. "miR-484 regulates mitochondrial network through targeting Fis1," Nature Communications, Nature, vol. 3(1), pages 1-9, January.
    • Handle: RePEc:nat:natcom:v:3:y:2012:i:1:d:10.1038_ncomms1770
    DOI: 10.1038/ncomms1770
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/ncomms1770
    File Function: Abstract
    Download Restriction: no
    File URL: https://libkey.io/10.1038/ncomms1770?utm_source=ideas
    LibKey link: if access is restricted and if your library uses this service, LibKey will redirect you to where you can use your library subscription to access this item
    ---><---

    Citations

    Citations are extracted by the CitEc Project, subscribe to its RSS feed for this item.
    as


    Cited by:

    1. Peter Langfelder & Fuying Gao & Nan Wang & David Howland & Seung Kwak & Thomas F Vogt & Jeffrey S Aaronson & Jim Rosinski & Giovanni Coppola & Steve Horvath & X William Yang, 2018. "MicroRNA signatures of endogenous Huntingtin CAG repeat expansion in mice," PLOS ONE, Public Library of Science, vol. 13(1), pages 1-20, January.
    2. Wang, Lan & Lang, Zimo & Duan, Jiayin & Zhang, Hanyu, 2023. "Heterogeneous venture capital and technological innovation network evolution: Corporate reputation as mediating variable," Finance Research Letters, Elsevier, vol. 51(C).

    More about this item

    Statistics

    Access and download statistics

    Corrections

    All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:natcom:v:3:y:2012:i:1:d:10.1038_ncomms1770. See general information about how to correct material in RePEc.

    If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.

    We have no bibliographic references for this item. You can help adding them by using this form .

    If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.

    For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .

    Please note that corrections may take a couple of weeks to filter through the various RePEc services.

    IDEAS is a RePEc service. RePEc uses bibliographic data supplied by the respective publishers.