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Published on: June 3, 2018
Reduction in trabecular meshwork stem cell content in donor eyes with primary open angle glaucoma
Yogapriya Sundaresan1, Lakshmi Priya Manivannan1, Shanthi Radhakrishnan2
1Department of Immunology and Stem Cell Biology, Aravind Medical Research Foundation, Madurai, 625020, Tamil Nadu, India.
Human trabecular meshwork stem cells (TMSCs) decline with age and in glaucoma. This study found significantly reduced TM cellularity and a trend towards lower TMSC content in glaucomatous eyes, suggesting a role in glaucoma pathogenesis.
Area of Science:
- Ophthalmology
- Stem Cell Biology
- Glaucoma Research
Background:
- Human trabecular meshwork stem cells (TMSCs) are characterized by high ABCG2/p75 expression and are crucial for trabecular meshwork (TM) health.
- Previous research indicated an age-related decrease in TMSC content, correlating with TM cell loss.
Purpose of the Study:
- To investigate the content of TMSCs in donor eyes with primary open angle glaucoma (POAG).
- To compare TM cellularity and TMSC levels in glaucomatous versus age-matched normal donor eyes.
Main Methods:
- Histopathological and immunostaining analyses were performed on anterior segments from glaucomatous (n=6) and normal (n=8) donor eyes.
- Quantification of total TM cells and TMSCs (ABCG2/p75 positive) was conducted using confocal microscopy and ImageJ software.
Main Results:
- Glaucomatous eyes exhibited significantly reduced TM cellularity (41.83 cells/section) compared to controls (69.33 cells/section).
- Structural changes in glaucomatous TM included thickened beams, fused trabeculae, and reduced Schlemm's canal dimensions.
- A non-significant trend of reduced TMSC percentage (0.14%) was observed in glaucomatous eyes compared to controls (4.73%).
Conclusions:
- The study confirms a significant decrease in TM cellularity in glaucomatous eyes.
- While a trend towards reduced TMSC content was noted, it was not statistically significant in this cohort.
- Further research is needed to clarify the role of TMSCs in the pathogenesis of primary open angle glaucoma.
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