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YAP determines the cell fate of injured mouse hepatocytes in vivo

Author

Listed:
  • Norio Miyamura

    (Medical Research Institute, Tokyo Medical and Dental University (TMDU))

  • Shoji Hata

    (Medical Research Institute, Tokyo Medical and Dental University (TMDU))

  • Tohru Itoh

    (Laboratory of Cell Growth and Differentiation, Institute of Molecular and Cellular Biosciences, The University of Tokyo)

  • Minoru Tanaka

    (Research Institute, National Center for Global Health and Medicine)

  • Miki Nishio

    (Kobe University Graduate School of Medicine)

  • Michiko Itoh

    (Graduate School of Medical and Dental Sciences)

  • Yoshihiro Ogawa

    (Graduate School of Medical and Dental Sciences, TMDU, AMED-CREST)

  • Shuji Terai

    (Graduate School of Medical and Dental Sciences, Niigata University)

  • Isao Sakaida

    (Graduate School of Medicine, Yamaguchi University)

  • Akira Suzuki

    (Kobe University Graduate School of Medicine)

  • Atsushi Miyajima

    (Laboratory of Cell Growth and Differentiation, Institute of Molecular and Cellular Biosciences, The University of Tokyo)

  • Hiroshi Nishina

    (Medical Research Institute, Tokyo Medical and Dental University (TMDU))

Abstract

The presence of senescent, transformed or damaged cells can impair tissue function or lead to tumorigenesis; therefore, organisms have evolved quality control mechanisms to eliminate them. Here, we show that YAP activation induced by inactivation of the Hippo pathway specifically in damaged hepatocytes promotes their selective elimination by using in vivo mosaic analysis in mouse liver. These damaged hepatocytes migrate into the hepatic sinusoids, undergo apoptosis and are engulfed by Kupffer cells. In contrast, YAP activation in undamaged hepatocytes leads to proliferation. Cellular stresses such as ethanol that damage both liver sinusoidal endothelial cells and hepatocytes switch cell fate from proliferation to migration/apoptosis in the presence of activated YAP. This involves the activation of CDC42 and Rac that regulate cell migration. Thus, we suggest that YAP acts as a stress sensor that induces elimination of injured cells to maintain tissue and organ homeostasis.

Suggested Citation

  • Norio Miyamura & Shoji Hata & Tohru Itoh & Minoru Tanaka & Miki Nishio & Michiko Itoh & Yoshihiro Ogawa & Shuji Terai & Isao Sakaida & Akira Suzuki & Atsushi Miyajima & Hiroshi Nishina, 2017. "YAP determines the cell fate of injured mouse hepatocytes in vivo," Nature Communications, Nature, vol. 8(1), pages 1-10, December.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms16017
    DOI: 10.1038/ncomms16017
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    Cited by:

    1. Nanase Igarashi & Kenichi Miyata & Tze Mun Loo & Masatomo Chiba & Aki Hanyu & Mika Nishio & Hiroko Kawasaki & Hao Zheng & Shinya Toyokuni & Shunsuke Kon & Keiji Moriyama & Yasuyuki Fujita & Akiko Taka, 2022. "Hepatocyte growth factor derived from senescent cells attenuates cell competition-induced apical elimination of oncogenic cells," Nature Communications, Nature, vol. 13(1), pages 1-11, December.

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