PuSH - Publikationsserver des Helmholtz Zentrums München

Zöller, M. ; Mastalerz, M. ; Dick, E. ; Merl-Pham, J. ; Hennen, E. ; Chakraborty, A. ; Nakayama, M. ; Klotz, M. ; Marchi, H. ; Le Gleut, R. ; Sadeleer, L.J.D.* ; Wuyts, W.A.* ; Vanaudenaerde, B.* ; Jeridi, A. ; Prasse, A.* ; Jäger, B.* ; Santofimia‐Castaño, P.* ; Stoleriu, M.-G. ; Hilgendorff, A. ; Hauck, S.M. ; Yildirim, A.Ö. ; Schiller, H.B. ; Staab-Weijnitz, C.A.

Nuclear protein 1 is a cell death regulator in primary human airway epithelial cells and reduced in idiopathic pulmonary fibrosis.

Sci. Rep. 16:14728 (2026)
Verlagsversion Forschungsdaten DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
The airway epithelium is the first site of injury from cigarette smoke (CS), a major risk factor for chronic lung disease including idiopathic pulmonary fibrosis (IPF). Here, we report the first intracellular proteomic analysis of CS exposure in fully differentiated primary human bronchial epithelial cells (phBECs). Following pathway enrichment analysis, we identified nuclear protein 1 (NUPR1) as a candidate regulator of epithelial stress responses. In contrast to the prediction by pathway enrichment analysis, NUPR1 activity was not altered by CS in vitro. Nevertheless, inhibition of its nuclear translocation using ZZW-115 revealed a cytoprotective and anti-apoptotic role in phBECs, as demonstrated by increased apoptosis and impaired epithelial integrity. NUPR1 expression was markedly reduced in IPF whole lung tissue and bronchial epithelium. IPF-derived basal cells differentiated into an epithelium exhibiting fewer ciliated and more secretory cells which exhibited significantly higher sensitivity to NUPR1 inhibition. Our findings underscore cell type- and tissue-specific variation in NUPR1-dependent pathways. Collectively, this study positions NUPR1 as a context-dependent epithelial stress regulator whose loss may contribute to epithelial vulnerability in IPF.
Altmetric
Weitere Metriken?
[➜Einloggen]
Zusatzinfos bearbeiten [➜Einloggen]
Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Idiopathic Pulmonary Fibrosis ; Regulator ; Epithelium ; Respiratory Epithelium ; Apoptosis ; Lung ; Intracellular ; Nuclear Protein
ISSN (print) / ISBN 2045-2322
e-ISSN 2045-2322
Zeitschrift Scientific Reports
Quellenangaben Band: 16, Heft: 1, Seiten: , Artikelnummer: 14728 Supplement: ,
Verlag Springer
Verlagsort London
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Lung Health and Immunity (LHI)
CF Metabolomics & Proteomics (CF-MPC)
Core Facility Bioinformatics and Statistics (CF-BIOS)
Research Unit Precision Regenerative Medicine (PRM)
Förderungen University of Colorado
European Research Council
Deutsche Forschungsgemeinschaft