RGD surface functionalization of the hydrophilic acrylic intraocular lens material to control posterior capsular opacification.
Identifieur interne : 000480 ( PubMed/Corpus ); précédent : 000479; suivant : 000481RGD surface functionalization of the hydrophilic acrylic intraocular lens material to control posterior capsular opacification.
Auteurs : Yi-Shiang Huang ; Virginie Bertrand ; Dimitriya Bozukova ; Christophe Pagnoulle ; Christine Labrugère ; Edwin De Pauw ; Marie-Claire De Pauw-Gillet ; Marie-Christine DurrieuSource :
- PloS one [ 1932-6203 ] ; 2014.
English descriptors
- KwdEn :
- Animals, Capsule Opacification (pathology), Capsule Opacification (surgery), Cataract (pathology), Cataract (therapy), Cataract Extraction (adverse effects), Cell Adhesion (drug effects), Cell Dedifferentiation (drug effects), Cell Line, Epithelial Cells (drug effects), Epithelial Cells (pathology), Epithelial-Mesenchymal Transition (drug effects), Humans, Lenses, Intraocular (adverse effects), Prostheses and Implants (adverse effects), Swine.
- MESH :
- adverse effects : Cataract Extraction, Lenses, Intraocular, Prostheses and Implants.
- drug effects : Cell Adhesion, Cell Dedifferentiation, Epithelial Cells, Epithelial-Mesenchymal Transition.
- pathology : Capsule Opacification, Cataract, Epithelial Cells.
- surgery : Capsule Opacification.
- therapy : Cataract.
- Animals, Cell Line, Humans, Swine.
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.
DOI: 10.1371/journal.pone.0114973
PubMed: 25501012
Links to Exploration step
pubmed:25501012Le document en format XML
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<term>Cataract (pathology)</term>
<term>Cataract (therapy)</term>
<term>Cataract Extraction (adverse effects)</term>
<term>Cell Adhesion (drug effects)</term>
<term>Cell Dedifferentiation (drug effects)</term>
<term>Cell Line</term>
<term>Epithelial Cells (drug effects)</term>
<term>Epithelial Cells (pathology)</term>
<term>Epithelial-Mesenchymal Transition (drug effects)</term>
<term>Humans</term>
<term>Lenses, Intraocular (adverse effects)</term>
<term>Prostheses and Implants (adverse effects)</term>
<term>Swine</term>
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<term>Lenses, Intraocular</term>
<term>Prostheses and Implants</term>
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<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Adhesion</term>
<term>Cell Dedifferentiation</term>
<term>Epithelial Cells</term>
<term>Epithelial-Mesenchymal Transition</term>
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<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Capsule Opacification</term>
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<term>Epithelial Cells</term>
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<front><div type="abstract" xml:lang="en">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.</div>
</front>
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<Abstract><AbstractText>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.</AbstractText>
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<MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000818">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName MajorTopicYN="N" UI="D058442">Capsule Opacification</DescriptorName>
<QualifierName MajorTopicYN="Y" UI="Q000473">pathology</QualifierName>
<QualifierName MajorTopicYN="N" UI="Q000601">surgery</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName MajorTopicYN="N" UI="D002386">Cataract</DescriptorName>
<QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName>
<QualifierName MajorTopicYN="Y" UI="Q000628">therapy</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName MajorTopicYN="N" UI="D002387">Cataract Extraction</DescriptorName>
<QualifierName MajorTopicYN="N" UI="Q000009">adverse effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName MajorTopicYN="N" UI="D002448">Cell Adhesion</DescriptorName>
<QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName MajorTopicYN="N" UI="D054337">Cell Dedifferentiation</DescriptorName>
<QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName MajorTopicYN="N" UI="D002460">Cell Line</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName MajorTopicYN="N" UI="D004847">Epithelial Cells</DescriptorName>
<QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName>
<QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName MajorTopicYN="N" UI="D058750">Epithelial-Mesenchymal Transition</DescriptorName>
<QualifierName MajorTopicYN="Y" UI="Q000187">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName MajorTopicYN="N" UI="D007910">Lenses, Intraocular</DescriptorName>
<QualifierName MajorTopicYN="Y" UI="Q000009">adverse effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName MajorTopicYN="N" UI="D019736">Prostheses and Implants</DescriptorName>
<QualifierName MajorTopicYN="N" UI="Q000009">adverse effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName MajorTopicYN="N" UI="D013552">Swine</DescriptorName>
</MeshHeading>
</MeshHeadingList>
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