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

Ke, Hengning; Masoumi, Katarzyna Chmielarska LU ; Ahlqvist, Kristofer LU ; Seckl, Michael J; Rydell-Törmänen, Kristina LU and Massoumi, Ramin LU (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
organization
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type
Contribution to journal
publication status
published
subject
in
Scientific Reports
volume
6
publisher
Nature Publishing Group
external identifiers
  • 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
2016-11-06 04:36:57
@misc{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    = {ARRAY(0x96800e8)},
  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},
  volume       = {6},
  year         = {2016},
}