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Self-renewing diploid Axin2+ cells fuel homeostatic renewal of the liver

Author

Listed:
  • Bruce Wang

    (Howard Hughes Medical Institute, Stanford Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine
    University of California San Francisco)

  • Ludan Zhao

    (Howard Hughes Medical Institute, Stanford Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine)

  • Matt Fish

    (Howard Hughes Medical Institute, Stanford Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine)

  • Catriona Y. Logan

    (Howard Hughes Medical Institute, Stanford Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine)

  • Roel Nusse

    (Howard Hughes Medical Institute, Stanford Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine)

Abstract

The source of new hepatocytes in the uninjured liver has remained an open question. By lineage tracing using the Wnt-responsive gene Axin2 in mice, we identify a population of proliferating and self-renewing cells adjacent to the central vein in the liver lobule. These pericentral cells express the early liver progenitor marker Tbx3, are diploid, and thereby differ from mature hepatocytes, which are mostly polyploid. The descendants of pericentral cells differentiate into Tbx3-negative, polyploid hepatocytes, and can replace all hepatocytes along the liver lobule during homeostatic renewal. Adjacent central vein endothelial cells provide Wnt signals that maintain the pericentral cells, thereby constituting the niche. Thus, we identify a cell population in the liver that subserves homeostatic hepatocyte renewal, characterize its anatomical niche, and identify molecular signals that regulate its activity.

Suggested Citation

  • Bruce Wang & Ludan Zhao & Matt Fish & Catriona Y. Logan & Roel Nusse, 2015. "Self-renewing diploid Axin2+ cells fuel homeostatic renewal of the liver," Nature, Nature, vol. 524(7564), pages 180-185, August.
    • Handle: RePEc:nat:nature:v:524:y:2015:i:7564:d:10.1038_nature14863
    DOI: 10.1038/nature14863
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    Cited by:

    1. M. L. Richter & I. K. Deligiannis & K. Yin & A. Danese & E. Lleshi & P. Coupland & C. A. Vallejos & K. P. Matchett & N. C. Henderson & M. Colome-Tatche & C. P. Martinez-Jimenez, 2021. "Single-nucleus RNA-seq2 reveals functional crosstalk between liver zonation and ploidy," Nature Communications, Nature, vol. 12(1), pages 1-16, December.
    2. Ana Belén Plata-Gómez & Lucía Prado-Rivas & Alba Sanz & Nerea Deleyto-Seldas & Fernando García & Celia Calle Arregui & Camila Silva & Eduardo Caleiras & Osvaldo Graña-Castro & Elena Piñeiro-Yáñez & Jo, 2024. "Hepatic nutrient and hormone signaling to mTORC1 instructs the postnatal metabolic zonation of the liver," Nature Communications, Nature, vol. 15(1), pages 1-19, December.
    3. Inmaculada Ruz-Maldonado & John T. Gonzalez & Hanming Zhang & Jonathan Sun & Alicia Bort & Inamul Kabir & Richard G. Kibbey & Yajaira Suárez & Daniel M. Greif & Carlos Fernández-Hernando, 2024. "Heterogeneity of hepatocyte dynamics restores liver architecture after chemical, physical or viral damage," Nature Communications, Nature, vol. 15(1), pages 1-23, December.

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