Inhibition of posterior capsule opacification with an immunotoxin specific for lens epithelial cells: 24 month clinical results

1998 ◽  
Vol 24 (12) ◽  
pp. 1614-1620 ◽  
Author(s):  
Donald S. Clark ◽  
Jared M. Emery ◽  
Mark E. Munsell
RSC Advances ◽  
2015 ◽  
Vol 5 (5) ◽  
pp. 3597-3604 ◽  
Author(s):  
Bailiang Wang ◽  
Quankui Lin ◽  
Tingwei Jin ◽  
Chenghui Shen ◽  
Junmei Tang ◽  
...  

Posterior capsule opacification is one of the complications of cataract surgery caused by the adhesion and reproduction of residual human lens epithelial cells (HLECs) on the posterior capsule.


2014 ◽  
Vol 8 (1) ◽  
pp. 19-23 ◽  
Author(s):  
Karin Sundelin ◽  
Anne Petersen ◽  
Yalda Soltanpour ◽  
Madeleine Zetterberg

Aim : Inter-individual differences in intrinsic proliferative capacity of lens epithelial cells may have importance for the risk of developing posterior capsule opacification (PCO) after cataract surgery. The purpose of the present study was to determine growth of human lens epithelial cells (HLEC) in culture and investigate possible associations with clinical characteristics of the donors, such as age, sex, pseudoexfoliation, uveitis and diabetes. Methods : Pieces of lens capsule and adhering lens epithelial cells were obtained through capsulorhexis at cataract surgery. Specimens were cultured in a humidified CO2-incubator using standard culture medium and 5% fetal calf serum for two weeks after which cultured cells were stained with carboxy-fluorescein diacetate succinimidyl ester. Image processing software was used to determine the area of the confluent epithelial cell layer in relation to the size of the original capsule specimen. Results : The increase in area of confluent HLEC showed a negative correlation with diabetes at the first week after surgery. Lower age and female sex showed border-line significant associations with a higher rate of cell proliferation. The presence of pseudoexfoliation in vivo did not significantly affect cell growth in culture postoperatively. Nor did installation of xylocain in the anterior chamber during surgery. Conclusion : Diabetes is associated with lower rate of proliferation of lens epithelial cells in culture. The lack of strong correlations between in vitro growth and known risk factors for PCO in the donors suggest that other factors than the proliferative capacity of the cells per se are important for PCO formation.


1999 ◽  
Vol 19 (6) ◽  
pp. 472-482 ◽  
Author(s):  
Bettina C. Couderc ◽  
Sylvie de Neuville ◽  
Victorine Douin-Echinard ◽  
Brigitte Serres ◽  
Stéphane Manenti ◽  
...  

2020 ◽  
Vol 477 (1) ◽  
pp. 75-97 ◽  
Author(s):  
Mi-Hyun Nam ◽  
Andrew J.O. Smith ◽  
Mina B. Pantcheva ◽  
Ko Uoon Park ◽  
Joseph A. Brzezinski ◽  
...  

Posterior capsule opacification (PCO) is a complication after cataract surgery that can disrupt vision. The epithelial to mesenchymal transition (EMT) of lens epithelial cells (LECs) in response to transforming growth factor β2 (TGFβ2) has been considered an obligatory mechanism for PCO. In this study, we tested the efficacy of aspirin in inhibiting the TGFβ2-mediated EMT of human LECs, LECs in human lens capsular bags, and lensectomized mice. In human LECs, the levels of the EMT markers α-smooth muscle actin (α-SMA) and fibronectin were drastically reduced by treatment with 2 mM aspirin. Aspirin also halted the EMT response of TGFβ2 when introduced after EMT initiation. In human capsular bags, treatment with 2 mM aspirin significantly suppressed posterior capsule wrinkling and the expression α-SMA in capsule-adherent LECs. The inhibition of TGFβ2-mediated EMT in human LECs was not dependent on Smad phosphorylation or MAPK and AKT-mediated signaling. We found that aspirin significantly increased the acetylation of K56 and K122 in histone H3 of human LECs. Chromatin immunoprecipitation assays using acetyl-H3K56 or acetyl-H3K122 antibody revealed that aspirin blocked the TGFβ2-induced acetylation of H3K56 and H3K122 at the promoter regions of ACTA2 and COL1A1. After lensectomy in mice, we observed an increase in the proliferation and α-SMA expression of the capsule-adherent LECs, which was ameliorated by aspirin administration through drinking water. Taken together, our results showed that aspirin inhibits TGFβ2-mediated EMT of LECs, possibly from epigenetic down-regulation of EMT-related genes.


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