Wnt3a regulates proliferation and migration of HUVEC via canonical and non-canonical Wnt signaling pathways
Abstract
Untangling the signaling pathways involved in endothelial cell biology is of central interest for the development of antiangiogenesis based therapies. Here we report that Wnt3a induces the proliferation and migration of HUVECs, but does not affect their survival. Wnt3a-induced proliferation was VEGFR signaling independent, but reduced upon CamKII inhibition. In a search for the downstream mediators of Wnt3a's effects on HUVEC biology, we found that Wnt3a treatment leads to phosphorylation of DVL3 and stabilization of {beta}-catenin. Moreover, under the same conditions we observed an upregulation in c-MYC, TIE-2 and GJA1 mRNA transcripts. Although treatment of HUVECs with Wnt5a induced DVL3 phosphorylation, we did not observe any of the other effects seen upon Wnt3a stimulation. Taken together, our data indicate that Wnt3a induces canonical and non-canonical Wnt signaling in HUVECs, and stimulates their proliferation and migration.
- Authors:
-
- Friedrich Miescher Institute for Biomedical Research, Basel (Switzerland)
- Cancer and Infection Research Area, AstraZeneca Pharmaceuticals, Macclesfield (United Kingdom)
- Bayer Schering Pharma AG, Wuppertal (Germany)
- Publication Date:
- OSTI Identifier:
- 22199773
- Resource Type:
- Journal Article
- Journal Name:
- Biochemical and Biophysical Research Communications
- Additional Journal Information:
- Journal Volume: 386; Journal Issue: 3; Other Information: Copyright (c) 2009 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
- Subject:
- 60 APPLIED LIFE SCIENCES; BIOLOGY; INHIBITION; MESSENGER-RNA; PHOSPHORYLATION; STABILIZATION; STIMULATION; THERAPY
Citation Formats
Samarzija, Ivana, Sini, Patrizia, Schlange, Thomas, MacDonald, Gwen, and Hynes, Nancy E., E-mail: Nancy.Hynes@fmi.ch. Wnt3a regulates proliferation and migration of HUVEC via canonical and non-canonical Wnt signaling pathways. United States: N. p., 2009.
Web. doi:10.1016/J.BBRC.2009.06.033.
Samarzija, Ivana, Sini, Patrizia, Schlange, Thomas, MacDonald, Gwen, & Hynes, Nancy E., E-mail: Nancy.Hynes@fmi.ch. Wnt3a regulates proliferation and migration of HUVEC via canonical and non-canonical Wnt signaling pathways. United States. https://doi.org/10.1016/J.BBRC.2009.06.033
Samarzija, Ivana, Sini, Patrizia, Schlange, Thomas, MacDonald, Gwen, and Hynes, Nancy E., E-mail: Nancy.Hynes@fmi.ch. 2009.
"Wnt3a regulates proliferation and migration of HUVEC via canonical and non-canonical Wnt signaling pathways". United States. https://doi.org/10.1016/J.BBRC.2009.06.033.
@article{osti_22199773,
title = {Wnt3a regulates proliferation and migration of HUVEC via canonical and non-canonical Wnt signaling pathways},
author = {Samarzija, Ivana and Sini, Patrizia and Schlange, Thomas and MacDonald, Gwen and Hynes, Nancy E., E-mail: Nancy.Hynes@fmi.ch},
abstractNote = {Untangling the signaling pathways involved in endothelial cell biology is of central interest for the development of antiangiogenesis based therapies. Here we report that Wnt3a induces the proliferation and migration of HUVECs, but does not affect their survival. Wnt3a-induced proliferation was VEGFR signaling independent, but reduced upon CamKII inhibition. In a search for the downstream mediators of Wnt3a's effects on HUVEC biology, we found that Wnt3a treatment leads to phosphorylation of DVL3 and stabilization of {beta}-catenin. Moreover, under the same conditions we observed an upregulation in c-MYC, TIE-2 and GJA1 mRNA transcripts. Although treatment of HUVECs with Wnt5a induced DVL3 phosphorylation, we did not observe any of the other effects seen upon Wnt3a stimulation. Taken together, our data indicate that Wnt3a induces canonical and non-canonical Wnt signaling in HUVECs, and stimulates their proliferation and migration.},
doi = {10.1016/J.BBRC.2009.06.033},
url = {https://www.osti.gov/biblio/22199773},
journal = {Biochemical and Biophysical Research Communications},
issn = {0006-291X},
number = 3,
volume = 386,
place = {United States},
year = {Fri Aug 28 00:00:00 EDT 2009},
month = {Fri Aug 28 00:00:00 EDT 2009}
}