IDEAS home Printed from https://ideas.repec.org/a/nat/nature/v517y2015i7536d10.1038_nature14112.html
   My bibliography  Save this article

Lineage-negative progenitors mobilize to regenerate lung epithelium after major injury

Author

Listed:
  • Andrew E. Vaughan

    (Cardiovascular Research Institute, University of California, San Francisco (UCSF), San Francisco, California 94143, USA)

  • Alexis N. Brumwell

    (Cardiovascular Research Institute, University of California, San Francisco (UCSF), San Francisco, California 94143, USA)

  • Ying Xi

    (Cardiovascular Research Institute, University of California, San Francisco (UCSF), San Francisco, California 94143, USA)

  • Jeffrey E. Gotts

    (Cardiovascular Research Institute, University of California, San Francisco (UCSF), San Francisco, California 94143, USA)

  • Doug G. Brownfield

    (Stanford University School of Medicine and Howard Hughes Medical Institute)

  • Barbara Treutlein

    (Max Planck Institute for Evolutionary Anthropology, Deutscher Platz 6, 04103 Leipzig, Germany)

  • Kevin Tan

    (Cardiovascular Research Institute, University of California, San Francisco (UCSF), San Francisco, California 94143, USA)

  • Victor Tan

    (Cardiovascular Research Institute, University of California, San Francisco (UCSF), San Francisco, California 94143, USA)

  • Feng Chun Liu

    (Cardiovascular Research Institute, University of California, San Francisco (UCSF), San Francisco, California 94143, USA)

  • Mark R. Looney

    (Cardiovascular Research Institute, University of California, San Francisco (UCSF), San Francisco, California 94143, USA)

  • Michael A. Matthay

    (Cardiovascular Research Institute, University of California, San Francisco (UCSF), San Francisco, California 94143, USA)

  • Jason R. Rock

    (School of Medicine, University of California, San Francisco (UCSF), San Francisco, California 94143, USA)

  • Harold A. Chapman

    (Cardiovascular Research Institute, University of California, San Francisco (UCSF), San Francisco, California 94143, USA)

Abstract

Lineage-tracing experiments identify a rare, undifferentiated population of quiescent cells in the mouse distal lung that are activated through a Notch signalling pathway to repair the epithelium after bleomycin- or influenza-mediated injury; inappropriate Notch signalling may be a major contributor to failed regeneration within the lungs of patients with chronic lung disease.

Suggested Citation

  • Andrew E. Vaughan & Alexis N. Brumwell & Ying Xi & Jeffrey E. Gotts & Doug G. Brownfield & Barbara Treutlein & Kevin Tan & Victor Tan & Feng Chun Liu & Mark R. Looney & Michael A. Matthay & Jason R. R, 2015. "Lineage-negative progenitors mobilize to regenerate lung epithelium after major injury," Nature, Nature, vol. 517(7536), pages 621-625, January.
  • Handle: RePEc:nat:nature:v:517:y:2015:i:7536:d:10.1038_nature14112
    DOI: 10.1038/nature14112
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/nature14112
    File Function: Abstract
    Download Restriction: Access to the full text of the articles in this series is restricted.

    File URL: https://libkey.io/10.1038/nature14112?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
    ---><---

    As the access to this document is restricted, you may want to search for a different version of it.

    Citations

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


    Cited by:

    1. Yuanyuan Chen & Reka Toth & Sara Chocarro & Dieter Weichenhan & Joschka Hey & Pavlo Lutsik & Stefan Sawall & Georgios T. Stathopoulos & Christoph Plass & Rocio Sotillo, 2022. "Club cells employ regeneration mechanisms during lung tumorigenesis," Nature Communications, Nature, vol. 13(1), pages 1-16, December.
    2. Benedikt Jaeger & Jonas Christian Schupp & Linda Plappert & Oliver Terwolbeck & Nataliia Artysh & Gian Kayser & Peggy Engelhard & Taylor Sterling Adams & Robert Zweigerdt & Henning Kempf & Stefan Lien, 2022. "Airway basal cells show a dedifferentiated KRT17highPhenotype and promote fibrosis in idiopathic pulmonary fibrosis," Nature Communications, Nature, vol. 13(1), pages 1-17, December.
    3. Yue Li & Pengzhen Dong & Yang Yang & Tianyu Guo & Quanyi Zhao & Dan Miao & Huanle Li & Tianfeng Lu & Fanning Xia & Jialan Lyu & Jun Ma & Thomas B. Kornberg & Qiang Zhang & Hai Huang, 2022. "Metabolic control of progenitor cell propagation during Drosophila tracheal remodeling," Nature Communications, Nature, vol. 13(1), pages 1-17, December.
    4. Andrew K. Beppu & Juanjuan Zhao & Changfu Yao & Gianni Carraro & Edo Israely & Anna Lucia Coelho & Katherine Drake & Cory M. Hogaboam & William C. Parks & Jay K. Kolls & Barry R. Stripp, 2023. "Epithelial plasticity and innate immune activation promote lung tissue remodeling following respiratory viral infection," Nature Communications, Nature, vol. 14(1), pages 1-16, December.
    5. Robert M. Cox & Josef D. Wolf & Nicole A. Lieberman & Carolin M. Lieber & Hae-Ji Kang & Zachary M. Sticher & Jeong-Joong Yoon & Meghan K. Andrews & Mugunthan Govindarajan & Rebecca E. Krueger & Elizab, 2024. "Therapeutic mitigation of measles-like immune amnesia and exacerbated disease after prior respiratory virus infections in ferrets," Nature Communications, Nature, vol. 15(1), pages 1-16, December.
    6. Richard J. Hewitt & Franz Puttur & David C. A. Gaboriau & Frédéric Fercoq & Maryline Fresquet & William J. Traves & Laura L. Yates & Simone A. Walker & Philip L. Molyneaux & Samuel V. Kemp & Andrew G., 2023. "Lung extracellular matrix modulates KRT5+ basal cell activity in pulmonary fibrosis," Nature Communications, Nature, vol. 14(1), pages 1-20, December.
    7. Laura Heydemann & Małgorzata Ciurkiewicz & Georg Beythien & Kathrin Becker & Klaus Schughart & Stephanie Stanelle-Bertram & Berfin Schaumburg & Nancy Mounogou-Kouassi & Sebastian Beck & Martin Zickler, 2023. "Hamster model for post-COVID-19 alveolar regeneration offers an opportunity to understand post-acute sequelae of SARS-CoV-2," Nature Communications, Nature, vol. 14(1), pages 1-19, December.
    8. Ning Yang & Joseph M. Luna & Peihong Dai & Yi Wang & Charles M. Rice & Liang Deng, 2022. "Lung type II alveolar epithelial cells collaborate with CCR2+ inflammatory monocytes in host defense against poxvirus infection," Nature Communications, Nature, vol. 13(1), pages 1-17, December.

    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:nature:v:517:y:2015:i:7536:d:10.1038_nature14112. 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.