Dataset Information

RGD surface functionalization of the hydrophilic acrylic intraocular lens material to control posterior capsular opacification.

ABSTRACT: Posterior Capsular Opacification (PCO) is the capsule fibrosis developed on implanted IntraOcular Lens (IOL) by the de-differentiation of Lens Epithelial Cells (LECs) undergoing Epithelial Mesenchymal Transition (EMT). Literature has shown that the incidence of PCO is multifactorial including the patient's age or disease, surgical technique, and IOL design and material. Reports comparing hydrophilic and hydrophobic acrylic IOLs have shown that the former has more severe PCO. On the other hand, we have previously demonstrated that the adhesion of LECs is favored on hydrophobic compared to hydrophilic materials. By combining these two facts and contemporary knowledge in PCO development via the EMT pathway, we propose a biomimetically inspired strategy to promote LEC adhesion without de-differentiation to reduce the risk of PCO development. By surface grafting of a cell adhesion molecule (RGD peptide) onto the conventional hydrophilic acrylic IOL material, the surface-functionalized IOL can be used to reconstitute a capsule-LEC-IOL sandwich structure, which has been considered to prevent PCO formation in literature. Our results show that the innovative biomaterial improves LEC adhesion, while also exhibiting similar optical (light transmittance, optical bench) and mechanical (haptic compression force, IOL injection force) properties compared to the starting material. In addition, compared to the hydrophobic IOL material, our bioactive biomaterial exhibits similar abilities in LEC adhesion, morphology maintenance, and EMT biomarker expression, which is the crucial pathway to induce PCO. The in vitro assays suggest that this biomaterial has the potential to reduce the risk factor of PCO development.

SUBMITTER: Huang YS

PROVIDER: S-EPMC4263720 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature

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Publications

RGD surface functionalization of the hydrophilic acrylic intraocular lens material to control posterior capsular opacification.

Huang Yi-Shiang YS Bertrand Virginie V Bozukova Dimitriya D Pagnoulle Christophe C Labrugère Christine C De Pauw Edwin E De Pauw-Gillet Marie-Claire MC Durrieu Marie-Christine MC

PloS one 20141211 12

Posterior Capsular Opacification (PCO) is the capsule fibrosis developed on implanted IntraOcular Lens (IOL) by the de-differentiation of Lens Epithelial Cells (LECs) undergoing Epithelial Mesenchymal Transition (EMT). Literature has shown that the incidence of PCO is multifactorial including the patient's age or disease, surgical technique, and IOL design and material. Reports comparing hydrophilic and hydrophobic acrylic IOLs have shown that the former has more severe PCO. On the other hand, w ...[more]

PMID: 25501012

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Project description:Cataract is the leading cause of visual impairment, and posterior capsular opacification (PCO) is the most common long-term complication of modern cataract surgery, which can cause severe visual impairment after surgery. The proliferation, migration, and epithelial-mesenchymal transition (EMT) of residual lens epithelial cells (LECs) stimulated by growth factors and cytokines, are the key pathological mechanisms involved in the development of PCO. This study demonstrated that non-steroidal anti-inflammatory drug (NSAID), bromfenac, was capable of effectively inhibiting cell migration, overexpression of EMT markers, such as fibronectin (FN), matrix metalloproteinase 2 (MMP2), α-smooth muscle actin (α-SMA), and transcription factor Snail, and extracellular signal-regulated kinase (ERK)/glycogen synthase kinase-3β (GSK-3β) signaling induced by transforming growth factor-β2 (TGF-β2) in vitro. The inhibitory effect of bromfenac on TGF-β2-induced EMT was also verified on a primary lens epithelial cell model using human anterior capsules. Furthermore, based on ultrasonic spray technology, we developed a drug-eluting intraocular lens (IOL) using poly (lactic-co-glycolic acid) (PLGA) with sustained bromfenac release ability for the prevention of PCO development. In the rabbit models of cataract surgery, bromfenac-eluting IOL exhibited remarkable PCO prevention and inflammation suppression effects with excellent biocompatibility. In conclusion, bromfenac can inhibit TGF-β2-induced cell migration and the EMT of LECs via ERK/GSK-3β/Snail signaling. The present study offers a novel approach for preventing PCO through PLGA-based drug sustained-release IOLs. Graphical abstract TGF-β2 promoted migration and EMT of lens epithelial cells (LECs) through activation of ERK/GSK-3β/Snail signaling, which could be suppressed by bromfenac. Novel bromfenac-based drug-eluting IOLs exhibited excellent PCO prevention in vivo.Image 1 Highlights • Bromfenac inhibited TGF-β2-induced migration and EMT of LECs through ERK/GSK-3β/Snail signaling.• Drug-eluting IOLs with sustained bromfenac release were developed based on ultrasonic spray technology.• Bromfenac-eluting IOLs exhibited remarkable PCO prevention and inflammation suppression effects in vivo.• Bromfenac-eluting IOLs hold great potential for clinical application of PCO prevention.

Dataset Information

RGD surface functionalization of the hydrophilic acrylic intraocular lens material to control posterior capsular opacification.

Publications

RGD surface functionalization of the hydrophilic acrylic intraocular lens material to control posterior capsular opacification.

Similar Datasets

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