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B. Amoozgar, H. Sheardown; Anti TGF-β2 and MMP Inhibitor Modification of PDMS as a Model IOL to Decrease the Incidence of PCO. Invest. Ophthalmol. Vis. Sci. 2010;51(13):4570.
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© ARVO (1962-2015); The Authors (2016-present)
Lens epithelial cells (LECs) remaining in the capsular bag following a cataract surgery, influenced by wound healing process, undergo epithelial to mesenchymal transition (EMT) and migrate from the anterior to posterior capsule resulting in the generation of fibroblastic cells, production of alpha smooth muscle actin (α-SMA), deposition of extracellular matrix (ECM), capsular wrinkling, and eventually posterior capsule opacification (PCO). The wound healing process is regulated by growth factors and cytokines especially transforming growth factor beta (TGF-β) and matrix metalloproteinases (MMPs). Delivery of TGF-β inhibitor (K16) or MMP inhibitors including sulfadiazine and tissue inhibitor of metalloproteinase (TIMP-3) via an intraocular lens (IOL) could prevent the cellular changes which lead to PCO by inhibition of EMT, ECM deposition, and migration of LECs.
The antibody and inhibitors were tethered to the surface of polydimethylsiloxane (PDMS), as a model lens material via a polyethylene glycol (PEG) spacer using a method previously established in our lab. The surfaces were characterized using ATR-FTIR, contact angles, XPS, and TOF-SIMS. Morphological properties were measured by profilometry and SEM. Human lens epithelial cell lines HLE-B3 and FHL 124 interactions with modified surfaces including the production of fibroblast marker α-SMA, ECM components fibronectin and laminin, and E-cadherin shedding were measured.
Surface modifications were confirmed by water contact angles and the presence of representative peaks in the ATR-FTIR, XPS, and TOF-SIMS. Cell viability measurement by MTT assay indicated more cell proliferation but less α-SMA and ECM components production in the presence of anti-TGF-β2 antibody (K16) compared to other inhibitors on the surface. However, tethering the inhibitors to the surface of PDMS led to decreased fibronectin and laminin deposition in the presence of exogenous TGF-β2.
Introduction of anti-TGF-β2 antibody and MMP inhibitors including sulfadiazine and TIMP-3 to the surface of PDMS as a model IOL reduced the production of α-SMA, fibronectin, and laminin by human LECs HLE-B3 and FHL 124 stimulated by TGF-β2. These modifications could be a potential indication for prevention of PCO.
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