Abstract
The prevention of the posterior capsule opacification is still unsolved. To interfere with proliferating cells the T-type calcium channel antagonist Mibefradil was immobilized in poly-lactic-co-glycolic-acid micro particles which were fixed at a capsular tension ring and tested in a human organ culture model as well as in human lens cells HLE-B3 in vitro. It is feasible to get a release significantly affecting cell viability and growth evaluated by MTT test and cell cycle analysis. In addition, Bionas® sensor chips were used for time-dependent adhesion experiments in living lens cells. Interestingly, the concentration of Mibefradil which inhibited subconfluent cells is not effective in confluent cells. This is an important feature for the protection of the intact tissue in the eye.
Highlights
Posterior capsule opacification (PCO) is still the major complication in cataract surgery in consequence of an activation of lens epithelial cells due to surgery [1,2,3,4] that involves cell phenotype changes [5], increased matrix production, proliferation and migration [6,7]
An inhibition of the calcium entry was found for platelet cells [15] but we provide evidence that our primary human lens epithelial cells in the cell culture express T-type calcium channels [16,17] as well as potassium channels [16,17,18], which were influenced by Mibefradil
In our new experiments we were interested in both, the time-dependent influence of Mibefradil on cell adhesion in subconfluent and confluent living cells in vitro and, we wanted to solve the question if this drug can be immobilized in PLGA micro particles which were affixed at a capsular tension ring as a practicable approach
Summary
Posterior capsule opacification (PCO) is still the major complication in cataract surgery in consequence of an activation of lens epithelial cells due to surgery [1,2,3,4] that involves cell phenotype changes [5], increased matrix production, proliferation and migration [6,7]. The mechanism of action of thapsigargin is to disable calcium signalling by depleting the ER calcium store, leading to cell cycle arrest [10]. Advances in the prevention of PCO have been made concerning the geometry of the intraocular lenses [11], sharp edged lenses were able to diminish the migration of lens cells [12, 13]. At least, this technique is not able to solve the long term problem of PCO [14]
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