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Modification of PDMS surface as a mo...

Amoozgar, Bahram.

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Modification of PDMS surface as a model lens material to prevent cellular changes associated with posterior capsule opacification (PCO).

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Modification of PDMS surface as a model lens material to prevent cellular changes associated with posterior capsule opacification (PCO)./
Author:	Amoozgar, Bahram.
Description:	170 p.
Notes:	Source: Dissertation Abstracts International, Volume: 72-08, Section: B, page: .
Contained By:	Dissertation Abstracts International72-08B.
Subject:	Biology, Cell. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=NR74588
ISBN:	9780494745885

Modification of PDMS surface as a model lens material to prevent cellular changes associated with posterior capsule opacification (PCO).
Amoozgar, Bahram.

Modification of PDMS surface as a model lens material to prevent cellular changes associated with posterior capsule opacification (PCO). - 170 p.

Source: Dissertation Abstracts International, Volume: 72-08, Section: B, page: .

Thesis (Ph.D.)--McMaster University (Canada), 2011.

Following cataract surgery, in which the opaque crystalline lens is removed and an artificial lens is implanted, the wound healing process initiated causes lens epithelial cells (LECs) remaining in the capsular bag to undergo epithelial to mesenchymal transition (EMT) and migrate from the anterior to the posterior capsule. This leads to the generation of fibroblastic cells, the accumulation of extracellular matrix (ECM) proteins, and formation of lenticular structure. Ultimately, the result of these processes is fibrosis, capsular wrinkling and eventually vision loss or posterior capsule opacification (PCO), known as the most common complication of a cataract surgery.

ISBN: 9780494745885Subjects--Topical Terms:

1017686
Biology, Cell.

Modification of PDMS surface as a model lens material to prevent cellular changes associated with posterior capsule opacification (PCO).
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035 $a (UMI)AAINR74588
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100 1 $a Amoozgar, Bahram. $3 1682477
245 1 0 $a Modification of PDMS surface as a model lens material to prevent cellular changes associated with posterior capsule opacification (PCO).
300 $a 170 p.
500 $a Source: Dissertation Abstracts International, Volume: 72-08, Section: B, page: .
502 $a Thesis (Ph.D.)--McMaster University (Canada), 2011.
520 $a Following cataract surgery, in which the opaque crystalline lens is removed and an artificial lens is implanted, the wound healing process initiated causes lens epithelial cells (LECs) remaining in the capsular bag to undergo epithelial to mesenchymal transition (EMT) and migrate from the anterior to the posterior capsule. This leads to the generation of fibroblastic cells, the accumulation of extracellular matrix (ECM) proteins, and formation of lenticular structure. Ultimately, the result of these processes is fibrosis, capsular wrinkling and eventually vision loss or posterior capsule opacification (PCO), known as the most common complication of a cataract surgery.
520 $a Transforming growth factor beta 2 (TGF-beta2) and matrix metalloproteinases (MMPs) play important roles in PCO, directly leading to EMT and migration of LECs. Therefore, in the current work, covalent modification of model lens materials with inhibitors to these molecules was investigated as a means of minimizing the incidence of PCO, reported in some studies to be as high as 40% after 5 years. Covalent binding of K16, an anti-TGF-beta 2 antibody, sulfadiazine, a novel MMP inhibitor (MMPI), reported herein for the first time, and TIMP3, a tissue inhibitor of metalloproteinases (TIMPs), which are natural inhibitors of MMPs, to the surface of the intraocular lens (IOL) material, might have the potential to mitigate or inhibit EMT and the subsequent events, consequently decreasing the incidence of PCO.
520 $a The K16, sulfadiazine, and TIMP3 were tethered to the surface of polydimethylsiloxane (PDMS) as a model lens material using a polyethylene glycol (PEG) spacer. Surfaces, characterized using a range of different methods, demonstrated successful modification. Addition of TGF-beta2 in the cell culture media induced the production of ECM components such as fibronectin and laminin, the EMT marker smooth muscle actin-alpha (alpha-SMA), led to the activation of migration marker Rho, and E-cadherin shedding by HLE-B3 and FHL124 cells. In most cases, these effects were decreased but not completely eradicated by the presence of anti-TGF-beta2 antibody (K16), sulfadiazine, and TIMP3 on the PDMS surfaces compared to unmodified PDMS and surfaces modified only with PEG, with sulfadiazine and to a lesser extent anti-TGF-beta2 showing the most promise. Therefore, these results suggest that IOL surface modification with sulfadiazine and anti-TGF-beta 2 antibody have more efficiency to reduce cellular changes associated with PCO.
590 $a School code: 0197.
650 4 $a Biology, Cell. $3 1017686
650 4 $a Health Sciences, Ophthalmology. $3 1019445
650 4 $a Engineering, Biomedical. $3 1017684
690 $a 0379
690 $a 0381
690 $a 0541
710 2 $a McMaster University (Canada). $3 1024893
773 0 $t Dissertation Abstracts International $g 72-08B.
790 $a 0197
791 $a Ph.D.
792 $a 2011
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=NR74588