Skip to content Skip to navigation
University of Warwick
  • Study
  • |
  • Research
  • |
  • Business
  • |
  • Alumni
  • |
  • News
  • |
  • About

University of Warwick
Publications service & WRAP

Highlight your research

  • WRAP
    • Home
    • Search WRAP
    • Browse by Warwick Author
    • Browse WRAP by Year
    • Browse WRAP by Subject
    • Browse WRAP by Department
    • Browse WRAP by Funder
    • Browse Theses by Department
  • Publications Service
    • Home
    • Search Publications Service
    • Browse by Warwick Author
    • Browse Publications service by Year
    • Browse Publications service by Subject
    • Browse Publications service by Department
    • Browse Publications service by Funder
  • Help & Advice
University of Warwick

The Library

  • Login
  • Admin

ERK5 is required for VEGF-mediated survival and tubular morphogenesis of primary human microvascular endothelial cells

Tools
- Tools
+ Tools

Roberts, Owain Llyr, Holmes, Katherine, Mueller, Juergen, Cross, Darren A. E. and Cross, Michael J. (2010) ERK5 is required for VEGF-mediated survival and tubular morphogenesis of primary human microvascular endothelial cells. Journal of Cell Science, Vol.123 (No.18). pp. 3189-3200. doi:10.1242/jcs.072801 ISSN 0021-9533.

Research output not available from this repository.

Request-a-Copy directly from author or use local Library Get it For Me service.

Official URL: http://dx.doi.org/10.1242/jcs.072801

Request Changes to record.

Abstract

Extracellular signal-regulated kinase 5 (ERK5) is activated in response to environmental stress and growth factors. Gene ablation of Erk5 in mice is embryonically lethal as a result of disruption of cardiovascular development and vascular integrity. We investigated vascular endothelial growth factor (VEGF)-mediated ERK5 activation in primary human dermal microvascular endothelial cells (HDMECs) undergoing proliferation on a gelatin matrix, and tubular morphogenesis within a collagen gel matrix. VEGF induced sustained ERK5 activation on both matrices. However, manipulation of ERK5 activity by siRNA-mediated gene silencing disrupted tubular morphogenesis without impacting proliferation. Overexpression of constitutively active MEK5 and ERK5 stimulated tubular morphogenesis in the absence of VEGF. Analysis of intracellular signalling revealed that ERK5 regulated AKT phosphorylation. On a collagen gel, ERK5 regulated VEGF-mediated phosphorylation of the pro-apoptotic protein BAD and increased expression of the anti-apoptotic protein BCL2, resulting in decreased caspase-3 activity and apoptosis suppression. Our findings suggest that ERK5 is required for AKT phosphorylation and cell survival and is crucial for endothelial cell differentiation in response to VEGF.

Item Type: Journal Article
Subjects: Q Science > QH Natural history > QH301 Biology
Divisions: Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School > Biomedical Sciences > Translational & Experimental Medicine > Metabolic and Vascular Health (- until July 2016)
Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School
Journal or Publication Title: Journal of Cell Science
Publisher: The Company of Biologists Ltd.
ISSN: 0021-9533
Official Date: 15 September 2010
Dates:
DateEvent
15 September 2010Published
Volume: Vol.123
Number: No.18
Number of Pages: 12
Page Range: pp. 3189-3200
DOI: 10.1242/jcs.072801
Status: Peer Reviewed
Publication Status: Published
Access rights to Published version: Restricted or Subscription Access
Funder: Biotechnology and Biological Sciences Research Council (Great Britain) (BBSRC), AstraZeneca, North West Cancer Research Fund (NWCRF)

Data sourced from Thomson Reuters' Web of Knowledge

Request changes or add full text files to a record

Repository staff actions (login required)

View Item View Item
twitter

Email us: wrap@warwick.ac.uk
Contact Details
About Us