Nemo-like kinase regulates the expression of vascular endothelial growth factor (VEGF) in alveolar epithelial cells
(2016) In Scientific Reports 6.- Abstract
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... (More)
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.
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- author
- Ke, Hengning ; Masoumi, Katarzyna Chmielarska LU ; Ahlqvist, Kristofer LU ; Seckl, Michael J ; Rydell-Törmänen, Kristina LU and Massoumi, Ramin LU
- organization
- publishing date
- 2016
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Scientific Reports
- volume
- 6
- article number
- 23987
- publisher
- Nature Publishing Group
- external identifiers
-
- pmid:27035511
- scopus:84963690602
- wos:000373208800001
- ISSN
- 2045-2322
- DOI
- 10.1038/srep23987
- language
- English
- LU publication?
- yes
- id
- 802ea41e-7b46-4641-acc7-63a33e71f6f1
- date added to LUP
- 2016-04-26 09:20:37
- date last changed
- 2024-05-31 02:09:51
@article{802ea41e-7b46-4641-acc7-63a33e71f6f1, abstract = {{<p>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.</p>}}, author = {{Ke, Hengning and Masoumi, Katarzyna Chmielarska and Ahlqvist, Kristofer and Seckl, Michael J and Rydell-Törmänen, Kristina and Massoumi, Ramin}}, issn = {{2045-2322}}, language = {{eng}}, publisher = {{Nature Publishing Group}}, series = {{Scientific Reports}}, title = {{Nemo-like kinase regulates the expression of vascular endothelial growth factor (VEGF) in alveolar epithelial cells}}, url = {{http://dx.doi.org/10.1038/srep23987}}, doi = {{10.1038/srep23987}}, volume = {{6}}, year = {{2016}}, }