Club cell-specific role of programmed cell death 5 in pulmonary fibrosis.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 34011956.
- Also identified by DOI 10.1038/s41467-021-23277-8 and PMC identifier 8134485.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
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.
Medical subject headings
- Apoptosis Regulatory Proteins
- Idiopathic Pulmonary Fibrosis
- Neoplasm Proteins