May 2003
Volume 44, Issue 13
ARVO Annual Meeting Abstract  |   May 2003
Placenta Growth Factor Upregulates VE-Cadherin Expression in Microvascular Endothelial Cells
Author Affiliations & Notes
  • J. Cai
    Optometry and Vision Sciences, Cardiff University, Cardiff, United Kingdom
  • M.E. Boulton
    Optometry and Vision Sciences, Cardiff University, Cardiff, United Kingdom
  • W.G. Jiang
    Surgery, University of Wales College of Medicine, Cardiff, United Kingdom
  • A. Ahmed
    Reproductive and Vascular Biology, University of Birmingham, Birmingham, United Kingdom
  • Footnotes
    Commercial Relationships  J. Cai, None; M.E. Boulton, None; W.G. Jiang, None; A. Ahmed, None.
  • Footnotes
    Support  Wellcome Trust
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 2874. doi:
  • Views
  • Share
  • Tools
    • Alerts
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      J. Cai, M.E. Boulton, W.G. Jiang, A. Ahmed; Placenta Growth Factor Upregulates VE-Cadherin Expression in Microvascular Endothelial Cells . Invest. Ophthalmol. Vis. Sci. 2003;44(13):2874.

      Download citation file:

      © ARVO (1962-2015); The Authors (2016-present)

  • Supplements

Abstract: : Purpose: We have previously reported that placenta growth factor (PlGF) plays an important role in the maintenance and remodelling of newly-formed vessel networks. The aim of this study was to determine if PlGF can regulate endothelial cell permeability and if this occurs through modulation of VE-cadherin. Methods: Retinal microvascular endothelial cells (BRMEC) were obtained from bovine eyes. Cultures were treated with 100ng/ml of either VEGF, PlGF or the VEGF:PlGF heterodimer for 0min, 5min, 1hr, 12hr and 24hr. Endothelial permeability was determined by monitoring transendothelial electrical resistance and FITC-dextran flux. Expression of VE-cadherin at both mRNA and protein level was determined using a combination of QRT-PCR, Western blotting and immunofluorescence staining. Results: As previously reported VEGF increased BRMEC permeability. A significant increase in permeability was noted as early as 5 min after addition of VEGF. By contrast, PlGF significant reduced permeability demonstrating a decrease in both transepithelial resistance and dextran flux. The VEGF:PlGF heterodimer had no significant effect on permeability. These results were consistent with the QRT-PCR data which showed a rapid (by 5 minutes post exposure) increase in VE-cadherin mRNA expression in cultures exposed to VEGF while mRNA levels were significantly reduced below those of controls in PlGF treated cells. Similarly, immunostaining demonstrated that VEGF causes a rapid decrease in VE-cadherin expression between endothelial cells after 5-minuntes treatment, whereas PlGF greatly increased VE-cadherin expression. The VEGF:PlGF heterodimer did not cause detectable changes in VE-cadherin expression between endothelial cells. Unexpectedly, Western blotting showed that overall expression of VE-cadherin did not change until 12 hours after addition of either VEGF or PlGF. After 12 hours, VEGF inhibited VE-cadherin expression, whereas PlGF increased VE-cadherin expression. This delay is likely to be due to both relocation and the phosphorylation status of VE-cadherin. Conclusions: PlGF reduces interendothelial permeability by upregulating VE-cadherin expression in microvascular endothelial cells. This is further confirmation that PlGF plays a critical role in pathological angiogenesis.

Keywords: growth factors/growth factor receptors • neovascularization • vascular cells 

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.