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Apoptosis and morphologic changes in drug-treated trabecular meshwork cells in vitro
S A Sibayan1, M A Latina, M E Sherwood
1Wellman Laboratories of Photomedicine, Massachusetts General Hospital, Harvard Medical School, Boston, USA.
Experimental Eye Research
|June 17, 1998
Summary
Certain anti-glaucoma medications like 5-fluorouracil, mitomycin-C, and epinephrine can induce apoptosis (programmed cell death) in trabecular meshwork cells. Timolol, pilocarpine, and dexamethasone did not cause apoptosis but induced other cellular changes.
Area of Science:
- Ophthalmology
- Cell Biology
- Pharmacology
Background:
- Glaucoma treatment often involves medications that affect the trabecular meshwork.
- Understanding cellular responses to these drugs is crucial for patient safety and treatment efficacy.
Purpose of the Study:
- To investigate the potential of anti-glaucoma drugs to induce apoptosis in bovine trabecular meshwork cells.
- To assess the effects of known apoptosis inducers and specific glaucoma medications on these cells.
Main Methods:
- In vitro culture of bovine trabecular meshwork cells.
- Exposure to varying concentrations of timolol, pilocarpine, epinephrine, 5-fluorouracil, mitomycin-C, and dexamethasone.
- Evaluation of apoptosis using phase-contrast microscopy, transmission electron microscopy, and in situ apoptosis labeling.
Main Results:
- 5-Fluorouracil, mitomycin-C, and epinephrine induced apoptosis in a dose- and time-dependent manner.
- Timolol, pilocarpine, and dexamethasone did not induce apoptosis.
- Timolol and pilocarpine caused secondary lysosome formation; dexamethasone increased mitochondria.
Conclusions:
- Trabecular meshwork cells can undergo apoptosis when exposed to 5-fluorouracil, mitomycin-C, and epinephrine.
- Timolol, pilocarpine, and dexamethasone do not induce apoptosis but cause significant morphological changes in trabecular meshwork cells.