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Autophagic dysregulation in glaucomatous trabecular meshwork cells
Kristine Porter1, Joshua Hirt1, W Daniel Stamer1
1Duke University, Department of Ophthalmology, Durham, NC, USA.
Biochimica Et Biophysica Acta
|December 9, 2014
Summary
Primary open angle glaucoma (POAG) involves cellular dysfunction in the trabecular meshwork (TM). Glaucomatous TM cells exhibit impaired autophagy, suggesting a key role in POAG progression.
Area of Science:
- Ophthalmology
- Cell Biology
- Molecular Biology
Background:
- Primary open angle glaucoma (POAG) is a degenerative eye disease linked to aging and elevated intraocular pressure (IOP).
- Elevated IOP in POAG results from increased resistance to aqueous humor (AH) outflow via the trabecular meshwork (TM).
- The molecular basis for this TM outflow resistance and associated cellular dysfunction remains largely unknown.
Purpose of the Study:
- To investigate autophagic function and response to oxidative stress in TM cells from POAG patients.
- To compare cellular dysfunction markers in TM cells from glaucomatous and age-matched donor eyes.
Main Methods:
- Isolation and culture of TM cells from glaucomatous and age-matched donor eyes.
- Assessment of senescence markers (SA-β-Gal, lipofuscin) and autophagic markers (LC3B-II, pRPS6K-T389).
- Evaluation of proteolysis and autophagy activation under hyperoxic conditions.
Main Results:
- Glaucomatous TM cells displayed increased SA-β-Gal and lipofuscin.
- Decreased LC3B-II levels and reduced proteolysis were observed in glaucomatous TM cells.
- Glaucomatous TM cells failed to activate autophagy in response to hyperoxic stress, indicating mTOR-dependent dysregulation.
Conclusions:
- Autophagic pathway dysregulation, particularly an impaired response to oxidative stress, is evident in TM cells from POAG patients.
- This impaired autophagic capacity may negatively affect TM tissue function, including mechanotransduction.
- Dysregulated autophagy represents a significant contributing factor to the progression of primary open angle glaucoma.
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