Main Projects

Epithelial cell plasticity in aging and fibrosis

  • Characterization of epithelial cell senescence in aging and IPF
  • Investigation of WISP1 signaling pathway in alveolar epithelial cells and human fibroblasts
  • Analysis of antifibrotic drug effects on epithelial cells
  • Characterization of single epithelial cell plasticity in aging and fibrosis

Alveolar epithelial cell phenotypes in lung repair and regeneration

  • Characterization of alveolar epithelial cell subtypes in murine mouse models and human chronic lung disease
  • Role of ATII cells in lung injury, repair and regeneration
  • Cell specific Wnt ligand/receptor driven epithelial cell repair in emphysema/COPD

Deciphering the role of non-canonical WNT signalling in the development and progression of chronic lung diseases

  • Examine the localization and expression of components of the Wnt signalling pathway in chronic lung diseases
  • Determine the contribution of beta-catenin-independent Wnt signaling to pathological features of emphysema/COPD and idiopathic pulmonary fibrosis
  • Investigate the (patho-)physiological effects of non-canonical Wnt signalling on pulmonary fibroblast biology and epithelial cell function

Functional characterization of receptor expression in remodeled airways of pulmonary fibrosis

Idiopathic pulmonary fibrosis (IPF) is a serious and life-threatening disease characterized by stiffening of the lung, leading to a progressive and irreversible decline in lung function. Although it is understood that IPF strongly affects the alveolar region, there is increasing evidence that airways are seriously impaired as well. This includes airway epithelial cell proliferation, differentiation, an increase of bronchioles in the distal lung, and altered function of conducting airways. I am interested in the identification of therapeutic targetable cell surface structures, which are altered in their expression and function in IPF. This project focuses on a surface receptor highly expressed on airway epithelial cells in IPF. It aims to identify the epithelial (sub)type mainly expressing this receptor and to further characterize the mechanism of altered expression in IPF. This project further researches the involvement of distinct pathways, such as TGF-β and Notch signaling, to a modified phenotype and potential signaling cross-talk.