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Accepted Manuscript
Research Article
Tetraspanin18 regulates angiogenesis through VEGFR2 and Notch pathways
Grace X. Li, Shaobing Zhang, Ren Liu, Bani Singh, Sukhmani Singh, David I. Quinn, Gage Crump, Parkash S. Gill
Biology Open 2020 : bio.050096 doi: 10.1242/bio.050096 Published 21 July 2020
Grace X. Li
1Department of Medicine, Keck School of Medicine of the University of Southern California, Los Angeles, California, USA
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Shaobing Zhang
1Department of Medicine, Keck School of Medicine of the University of Southern California, Los Angeles, California, USA
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Ren Liu
2Department of Medicine, USC Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA
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Bani Singh
1Department of Medicine, Keck School of Medicine of the University of Southern California, Los Angeles, California, USA
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Sukhmani Singh
3Department of Medicine, USC Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA
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David I. Quinn
1Department of Medicine, Keck School of Medicine of the University of Southern California, Los Angeles, California, USA
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Gage Crump
4Department of Neurobiology, Keck School of Medicine of the University of Southern California, Los Angeles, California, USA
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Parkash S. Gill
1Department of Medicine, Keck School of Medicine of the University of Southern California, Los Angeles, California, USA
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  • For correspondence: parkashg@med.usc.edu
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Abstract

The VEGF pathway is critically required for vasculogenesis, the formation of the primary vascular network. It is also required for angiogenesis resulting in sprouting and pruning of vessels to generate mature arborizing structures. The Notch pathway is essential for arterial-venous specification and the maturation of nascent vessels. We have determined that Tspan18, a member of the Tetraspanin family, is expressed in developing vessels but not mature vasculature in zebrafish and mouse wound healing. Moreover, reduction at Tspan18 level resulted in aberrant vascular patterning, impaired vessel stability, and defective arterial-venous specification. Tspan18 deficiency reduced VEGF, VEGFR2, Notch3, EphrinB2, and increased EphB4, VEGFR3, Semaphorin3, Neuropilin, and PlexinD1 expression. Furthermore, vascular defects of Tspan18 deficiency could be rescued by ectopic expression of VEGFR2 and Notch, but not by knockdown of Semaphorin or Plexin. Functional studies showed that knockdown of Tspan18 led to reduced endothelial cell migration, invasion, and tube formation. Tspan18 has dynamic expression, regulates vascular development and maturation in the embryo with re-expression in adult life in wound healing.

  • Received December 12, 2019.
  • Accepted February 27, 2020.
  • © 2020. Published by The Company of Biologists Ltd
http://creativecommons.org/licenses/by/4.0

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.

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Keywords

  • Tspan18
  • VEGFR2
  • NOTCH
  • Angiogenesis
  • Zebrafish

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Accepted Manuscript
Research Article
Tetraspanin18 regulates angiogenesis through VEGFR2 and Notch pathways
Grace X. Li, Shaobing Zhang, Ren Liu, Bani Singh, Sukhmani Singh, David I. Quinn, Gage Crump, Parkash S. Gill
Biology Open 2020 : bio.050096 doi: 10.1242/bio.050096 Published 21 July 2020
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Accepted Manuscript
Research Article
Tetraspanin18 regulates angiogenesis through VEGFR2 and Notch pathways
Grace X. Li, Shaobing Zhang, Ren Liu, Bani Singh, Sukhmani Singh, David I. Quinn, Gage Crump, Parkash S. Gill
Biology Open 2020 : bio.050096 doi: 10.1242/bio.050096 Published 21 July 2020

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