YAP determines the cell fate of injured mouse hepatocytes in vivo

Norio Miyamura, Shoji Hata, Tohru Itoh, Minoru Tanaka, Miki Nishio, Michiko Itoh, Yoshihiro Ogawa, Shuji Terai, Isao Sakaida, Akira Suzuki, Atsushi Miyajima and Hiroshi Nishina ()
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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)

Nature Communications, 2017, vol. 8, issue 1, 1-10

Abstract: 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.

Date: 2017
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DOI: 10.1038/ncomms16017

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