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Trabecular Meshwork Response to Pressure Elevation in the Living Human Eye

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Epigallocatechin-3-Gallate Protects Trabecular Meshwork Cells from Endoplasmic Reticulum Stress.

Linbin Zhou¹, Jing Na He¹, Lin Du¹

¹Department of Ophthalmology & Visual Sciences, The Chinese University of Hong Kong, Hong Kong.

Oxidative Medicine and Cellular Longevity

|November 21, 2022

Summary

Epigallocatechin-3-gallate (EGCG) protects trabecular meshwork (TM) cells from endoplasmic reticulum (ER) stress, a key factor in primary open-angle glaucoma (POAG). This green tea component shows promise as a novel therapeutic for POAG.

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A Magnetic Microbead Occlusion Model to Induce Ocular Hypertension-Dependent Glaucoma in Mice

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Published on: March 23, 2016

Area of Science:

Ophthalmology
Cell Biology
Pharmacology

Background:

Primary open-angle glaucoma (POAG) is linked to elevated intraocular pressure (IOP).
Trabecular meshwork (TM) cell dysfunction due to endoplasmic reticulum (ER) stress increases AH outflow resistance, raising IOP.
Epigallocatechin-3-gallate (EGCG), a green tea polyphenol, is known to alleviate ER stress but its role in TM cells is unexplored.

Purpose of the Study:

To investigate the potential of EGCG in mitigating tunicamycin-induced ER stress in TM cells.
To evaluate EGCG's protective effects on human TM (HTM) and primary porcine TM (PTM) cells.

Main Methods:

Cell viability was assessed using MTT assays for HTM and PTM cells.
ER stress markers (ATF4, HSPA5, DDIT3) were quantified using quantitative real-time PCR.
Primary porcine TM cells were characterized via immunostaining.

Main Results:

EGCG (40 µM and 80 µM) significantly enhanced HTM cell survival under tunicamycin-induced ER stress.
EGCG (40 µM) reduced the expression of ER stress markers in HTM cells.
EGCG (40 µM) decreased ER stress marker mRNA levels and improved cell viability in primary PTM cells.

Conclusions:

EGCG effectively protects TM cells from ER stress.
EGCG presents a potential therapeutic strategy for managing POAG by alleviating ER stress in TM cells.