Growth factor restriction impedes progression of wound healing following cataract surgery: identification of VEGF as a putative therapeutic target

Eldred, Julie A., McDonald, Matthew, Wilkes, Helen S., Spalton, David J. and Wormstone, I. Michael ORCID: https://orcid.org/0000-0002-6423-7766 (2016) Growth factor restriction impedes progression of wound healing following cataract surgery: identification of VEGF as a putative therapeutic target. Scientific Reports, 6. ISSN 2045-2322

Preview

PDF (Eldred et al - SciRep 2016) - Published Version Available under License Creative Commons Attribution. Download (2MB) | Preview

Abstract

Secondary visual loss occurs in millions of patients due to a wound-healing response, known as posterior capsule opacification (PCO), following cataract surgery. An intraocular lens (IOL) is implanted into residual lens tissue, known as the capsular bag, following cataract removal. Standard IOLs allow the anterior and posterior capsules to become physically connected. This places pressure on the IOL and improves contact with the underlying posterior capsule. New open bag IOL designs separate the anterior capsule and posterior capsules and further reduce PCO incidence. It is hypothesised that this results from reduced cytokine availability due to greater irrigation of the bag. We therefore explored the role of growth factor restriction on PCO using human lens cell and tissue culture models. We demonstrate that cytokine dilution, by increasing medium volume, significantly reduced cell coverage in both closed and open capsular bag models. This coincided with reduced cell density and myofibroblast formation. A screen of 27 cytokines identified nine candidates whose expression profile correlated with growth. In particular, VEGF was found to regulate cell survival, growth and myofibroblast formation. VEGF provides a therapeutic target to further manage PCO development and will yield best results when used in conjunction with open bag IOL designs.

Item Type:	Article
Additional Information:	This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
Uncontrolled Keywords:	epithelial-mesenchymal transition,lens diseases,experimental models of disease,mechanisms of disease,molecular medicine
Faculty \ School:	Faculty of Science > School of Biological Sciences Faculty of Science > School of Natural Sciences
UEA Research Groups:	Faculty of Science > Research Groups > Cells and Tissues
Depositing User:	Pure Connector
Date Deposited:	27 Apr 2016 13:00
Last Modified:	27 Jan 2024 02:46
URI:	https://ueaeprints.uea.ac.uk/id/eprint/58426
DOI:	10.1038/srep24453

Downloads

Actions (login required)

View Item