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High intraocular pressure (IOP) is a major risk factor for glaucoma. Resistance to outflow of aqueous humor through the trabecular meshwork cells (HTMCs) is believed to cause high IOP. However, the exact mechanism is unknown. IOP is known to fluctuate throughout the day, with much greater fluctuations in glaucomatous compared to normal eyes. These fluctuations cause a continual stretching of the trabecular meshwork. The aim of the study is to develop a dose- and time-response relationship between degree of stretch and HTMCs viability as well as to study specific downstream effects of mechanical stretch on changes in gap junction Connexin43 expression. Gap junctions are known to be important structural and functional intercellular channels in HTMCs. METHODS: HTMCs from various donors were obtained and grown in primary culture. Upon reaching near-confluency, HTMCs were stretched at 5%, 10%, and 15%, each for 24hr, 48hr, 72hr. Cell health was then measured using vital Trypan blue stain, lactate dehydrogenase (LDH) assay, and ELISA apoptosis assay. Expression of connexin43 was measured using real time qPCR and western blotting.


Mechanical Stress on Trabecular Meshwork