miR-182 and Trabecular Meshwork Dysfunction in High Tension Glaucoma

Principal Investigator

Project Goals

Primary open-angle glaucoma (POAG) is the most common type of glaucoma and lowering eye pressure is the main approach to treating POAG in the clinic. The purpose of this project is to study how a short RNA molecule known as miR-182 may affect the outflow of aqueous humor, which is the clear liquid circulating in the front part of human eyes to bathe its lens and other delicate tissue. We will examine how this short RNA affects eye pressure using an integrative approach. This study may generate therapeutic targets to control eye pressure in human glaucoma patients with high eye pressure.

Project Summary

Our goal is to study how a short RNA molecule called microRNA-182 (miR-182) may affect the exit of the clear liquid in the front part of human eyes (i.e., aqueous humor). Our preliminary studies have indicated that elevated expression of miR-182 may be associated with primary open-angle glaucoma (POAG) with high eye pressure. First, using human ocular cells derived from eye tissue, we will study how the increased expression of miR-182 affects the cellular functions related to the exit of aqueous humor. We will use high throughput RNA sequencing to identify the potential targets of miR-182 in these cells since these targets may play a role in POAG. Second, we will study how the increased expression of miR-182 may affect the secretion of nanoparticles known as exosomes from human ocular cells. We will characterize any potential alterations in the contents of these secreted exosomes, which are secreted directly into the aqueous humor. This project applies an integrative approach by combining multiple experimental technologies to examine the secretion of nanoparticles from glaucoma-related human cells. Successful completion of this comprehensive study will further reveal the role of miR-182 in glaucoma pathogenesis and may provide therapeutic targets for this common eye disorder.

First published on: July 14, 2016

Last modified on: December 27, 2024