Glaucomatous cell derived matrices differentially modulate non-glaucomatous trabecular meshwork cellular behavior.

ABSTRACT: Ocular hypertension is a causal risk-factor to developing glaucoma. This is associated with stiffening of the trabecular meshwork (TM), the primary site of resistance to aqueous-humor-outflow. The mechanisms underlying this stiffening or how pathologic extracellular matrix (ECM) affects cell function are poorly understood. It is recognized that mechanotransduction systems allow cells to sense and translate the intrinsic biophysical properties of ECM into intracellular signals to control gene transcription, protein expression, and cell behavior. Using an anterior segment perfusion model, we document that there are significantly more low flow regions that are much stiffer, and fewer high flow regions that are less stiff in glaucomatous TM (GTM) when compared to non-glaucomatous TMs (NTM). GT

SUBMITTER: Raghunathan VK 

PROVIDER: S-EPMC5899949 | biostudies-literature | 2018 Apr

REPOSITORIES: biostudies-literature