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B. Amoozgar, H. Sheardown; Surface Modification of PDMS With Anti-TGF-β2 Antibody Decreases TGF-β2-Stimulated Production of ECM Components and Minimizes Lens Cell Adhesion. Invest. Ophthalmol. Vis. Sci. 2008;49(13):2772.
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© ARVO (1962-2015); The Authors (2016-present)
Posterior capsule opacification (PCO) is the most common complication of cataract surgery. Cellular components remaining in the capsular bag following surgery can migrate from the anterior to the posterior capsule. Visual loss occurs as a result of migration of lens epithelial cells (LECs) associated with epithelial to mesenchymal transition (EMT), fibrosis, and wrinkling of the posterior capsule. Transforming growth factor beta 2 (TGF-β2) has been shown to play a role in EMT. TGF-β2 stimulates secretion of MMP-2 and MMP-9 which have in turn been implicated in PCO. A reliable method of inhibiting EMT of LECs may eventually minimize or eliminate the formation of PCO. Delivery of anti TGF-β2 antibody via intraocular lens (IOL) may allow for concentration at the site of the potentially proliferating cells.
Using a previously established method, the surface of polydimethylsiloxane (PDMS) as a model lens material was modified to introduce functional polyethylene glycol (PEG) to the surface. Subsequent replacement of OH terminus of the PEG with functional NHS group allowed for reaction with anti TGF-β2 antibody. The surface was characterized using ATR-FTIR, contact angle, XPS, and TOF-SIMS. Surface morphological properties were measured by AFM. Interactions of the modified surfaces with human lens epithelial cell lines HLE-B3 and FHL124 were examined. Specifically, the expression of proteins related to fibroblast phenotype was examined with and without TGF-β2 stimulation.
Surface modification was confirmed by changes in water contact angles and the presence of representative peaks in the XPS and ATR-FTIR. Cells viability measured by MTT assay demonstrated that the presence of antibody on the surface of these materials did not significantly alter cellular function. However, TGF-β2 stimulated production of ECM components by HLE-B3 and FHL124 cells such as collagen I and IV, α-smooth muscle actin (α-SMA), and fibronectin, measured via immunofluorescence was found to be decreased by the presence of the anti TGF-β2 antibody on the surface of these materials. This resulted in lower HLE-B3 and FHL124 cells adhesion.
TGF-β2 promoted HLE-B3 and FHL124 cells adhesion by inducing ECM components including collagen I and IV, fibronectin, and α-SMA. Introduction of anti TGF-β2 antibody on the PDMS model IOL surface inhibits the production of these TGF-β2 induced ECM components resulting in a decrease in HLE-B3 and FHL124 cell adhesion. This method of surface modification could be a potential indication for the prevention of PCO.
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