한빛사논문
- 조회1,423
Soo-Yeon Park1,7, Jung Yeon Hong2,7, Soo Yeon Lee1, Seung-Hyun Lee1, Mi Jeong Kim1, Soo Yeon Kim2, Kyung Won Kim2, Hyo Sup Shim3, Moo Suk Park4, Chun Geun Lee5,6, Jack A. Elias5, Myung Hyun Sohn2,* & Ho-Geun Yoon1,*
1Department of Biochemistry and Molecular Biology, Severance Medical Research Institute, Brain Korea 21 PLUS Project for Medical Sciences, Yonsei University College of Medicine, Seoul, Korea.
2Department of Pediatrics and Institute of Allergy, Severance Medical Research Institute, Brain Korea 21 PLUS Project for Medical Sciences, Yonsei University College of Medicine, Seoul, Korea.
3Department of Pathology, Yonsei University College of Medicine, Seoul, Korea.
4Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea.
5Molecular Microbiology and Immunology, Brown University, Providence, RI, USA.
6Department of Internal Medicine, Hanyang University, Seoul, Korea.
7These authors contributed equally: Soo-Yeon Park, Jung Yeon Hong.
*Corresponding author.
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.
논문정보
- Research article
- 2021년 05월 (BRIC 등록일 2021-05-26)
- 국내(교신)+국외 연구진
- 의약학 > 분자세포의학
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