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Club cell-specific role of programmed cell death 5 in pulmonary fibrosis

Author

Listed:
  • Soo-Yeon Park

    (Yonsei University College of Medicine)

  • Jung Yeon Hong

    (Yonsei University College of Medicine)

  • Soo Yeon Lee

    (Yonsei University College of Medicine)

  • Seung-Hyun Lee

    (Yonsei University College of Medicine)

  • Mi Jeong Kim

    (Yonsei University College of Medicine)

  • Soo Yeon Kim

    (Yonsei University College of Medicine)

  • Kyung Won Kim

    (Yonsei University College of Medicine)

  • Hyo Sup Shim

    (Yonsei University College of Medicine)

  • Moo Suk Park

    (Yonsei University College of Medicine)

  • Chun Geun Lee

    (Brown University
    Hanyang University)

  • Jack A. Elias

    (Brown University)

  • Myung Hyun Sohn

    (Yonsei University College of Medicine)

  • Ho-Geun Yoon

    (Yonsei University College of Medicine)

Abstract

Idiopathic pulmonary fibrosis (IPF) causes progressive fibrosis and worsening pulmonary function. Prognosis is poor and no effective therapies exist. We show that programmed cell death 5 (PDCD5) expression is increased in the lungs of patients with IPF and in mouse models of lung fibrosis. Lung fibrosis is significantly diminished by club cell-specific deletion of Pdcd5 gene. PDCD5 mediates β-catenin/Smad3 complex formation, promoting TGF-β-induced transcriptional activation of matricellular genes. Club cell Pdcd5 knockdown reduces matricellular protein secretion, inhibiting fibroblast proliferation and collagen synthesis. Here, we demonstrate the club cell-specific role of PDCD5 as a mediator of lung fibrosis and potential therapeutic target for IPF.

Suggested Citation

  • Soo-Yeon Park & Jung Yeon Hong & Soo Yeon Lee & Seung-Hyun Lee & Mi Jeong Kim & Soo Yeon Kim & Kyung Won Kim & Hyo Sup Shim & Moo Suk Park & Chun Geun Lee & Jack A. Elias & Myung Hyun Sohn & Ho-Geun Y, 2021. "Club cell-specific role of programmed cell death 5 in pulmonary fibrosis," Nature Communications, Nature, vol. 12(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-23277-8
    DOI: 10.1038/s41467-021-23277-8
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