Nemo-like kinase regulates the expression of vascular endothelial growth factor (VEGF) in alveolar epithelial cells

Summary, in English

The canonical Wnt signaling can be silenced either through β-catenin-mediated ubiquitination and degradation or through phosphorylation of Tcf and Lef by nemo-like kinase (NLK). In the present study, we generated NLK deficient animals and found that these mice become cyanotic shortly before death because of lung maturation defects. NLK-/- lungs exhibited smaller and compressed alveoli and the mesenchyme remained thick and hyperplastic. This phenotype was caused by epithelial activation of vascular endothelial growth factor (VEGF) via recruitment of Lef1 to the promoter of VEGF. Elevated expression of VEGF and activation of the VEGF receptor through phosphorylation promoted an increase in the proliferation rate of epithelial and endothelial cells. In summary, our study identifies NLK as a novel signaling molecule for proper lung development through the interconnection between epithelial and endothelial cells during lung morphogenesis.

• Author: Hengning Ke; Katarzyna Chmielarska Masoumi; Kristofer Ahlqvist; Michael J Seckl; Kristina Rydell-Törmänen; Ramin Massoumi
• Department/s: Department of Laboratory Medicine; Lung Biology; BioCARE: Biomarkers in Cancer Medicine improving Health Care, Education and Innovation
• Publishing year: 2016
• Language: English
• Publication/Series: Scientific Reports
• Volume: 6
• Links: http://dx.doi.org/10.1038/srep23987
• Document type: Journal article
• Publisher: Nature Publishing Group
• Topic: Cell and Molecular Biology
• Status: Published
• Research group: Lung Biology
• ISBN/ISSN/Other: ISSN: 2045-2322