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Bart M. Vanaudenaerde on Muck Rack

Bart M. Vanaudenaerde

As seen in: Nature, Cell Reports Physical Science, The Lancet, European Respiratory Journal, Chest
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Articles

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

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By Michal Mastalerz, Elisabeth Dick, Juliane Merl-Pham, Ashesh Chakraborty, Misako Nakayama, Markus Klotz, Laurens J. De Sadeleer, Wim Wuyts, Bart M. Vanaudenaerde, Antje Prasse, Benedikt Jäger, Patricia Santofimia-Castaño, Anne Hilgendorff, Stefanie Hauck, Herbert Schiller, Claudia A. Staab-Weijnitz, Marie Zöller, Elisabeth Hennen, Hannah Marchi, Ronan LeGleut, Aicha Jeridi, Mircea-Gabriel Stoleriu, Ali Ö. Yildirim
| Nature Verified
Abstract 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.
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Stability of freestanding lung surfactant films under simulated breathing conditions

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By Maria C. Novaes-Silva, Ainhoa Collada, Jesús Pérez-Gil, Bart M. Vanaudenaerde, Jan Vermant, Benjamin Buhl
| Cell Reports Physical Science Verified
Results and discussion Bastacky and Goerke, using low-temperature SEM, suggested that a continuous thin liquid film coats the alveolar walls and extends through the interalveolar pores.30 Upon inhalation, the alveoli expand, potentially stretching the pores and thinning the film. However, imaging such structures under dynamic conditions remains challenging.
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Single-cell atlas of human lung aging identifies cell type dyssynchrony and increased transcriptional entropy - Nature Communications

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By Ruben De Man, Taylor Adams, Edward Manning, Juan Garcia, Juan García Verified, Cristian Coarfa, Qi Song, Ziv Bar-Joseph, Bart M. Vanaudenaerde, Xiting Yan
| Nature Verified
Abstract Age is a major risk factor for lung disease. We characterized the changing cellular, transcriptional, and genomic landscape of human lung aging using single-cell RNA sequencing. We find that lung aging is cell-type dyssynchronous, with alveolar epithelial and endothelial cells exhibiting the greatest transcriptional changes. Among alveolar epithelial cells, aging is associated with a decreased relative proportion of surfactant-expressing SPChigh AT2 cells.
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