The Primary Open-Angle Glaucoma (POAG) is a neurodegenerative disease and its clinical out-comes lead to visual field constriction and blindness. The POAG etiology is very complex and its pathogenesis is mainly explained through both mechanical and vascular theories. The trabecular meshwork (TM), the most sensitive tissue of the eye anterior segment to oxidative stress (OS), is the main tissue involved in early stage POAG characterized by an increase in pressure. Preclini-cal assessment of neuroprotective drugs on animal models has not always shown correspond-ence with human clinical studies. In addition, the intra-ocular pressure management after a glaucoma diagnosis, does not always prevent blindness. Recently, we have been developing an innovative in vitro 3D-advanced human trabecular cell model on a millifluidic-platform as a tool to improve glaucoma studies. Herein, we analyze the effects of prolonged increased pres-sure alone and, in association with OS, on such in vitro platform. Moreover, we verify if such damaged TM triggers apoptosis on neuron like cells. Preliminary results show that TM cells are less sensitive to pressure elevation than OS, and OS-damaging effects were worsened by the pressure increase. The stressed TM releases harmful signals which increase apoptosis stimuli on neuron-like cells, suggesting its pivotal role in the glaucoma cascade.
An innovative in vitro open-angle glaucoma model (IVOM) shows changes induced by increased ocular pressure and oxi-dative stress
Vernazza S;Tirendi S;Passalacqua M.;Piacente F.;Scarfi S.;Bassi Anna Maria
2021-01-01
Abstract
The Primary Open-Angle Glaucoma (POAG) is a neurodegenerative disease and its clinical out-comes lead to visual field constriction and blindness. The POAG etiology is very complex and its pathogenesis is mainly explained through both mechanical and vascular theories. The trabecular meshwork (TM), the most sensitive tissue of the eye anterior segment to oxidative stress (OS), is the main tissue involved in early stage POAG characterized by an increase in pressure. Preclini-cal assessment of neuroprotective drugs on animal models has not always shown correspond-ence with human clinical studies. In addition, the intra-ocular pressure management after a glaucoma diagnosis, does not always prevent blindness. Recently, we have been developing an innovative in vitro 3D-advanced human trabecular cell model on a millifluidic-platform as a tool to improve glaucoma studies. Herein, we analyze the effects of prolonged increased pres-sure alone and, in association with OS, on such in vitro platform. Moreover, we verify if such damaged TM triggers apoptosis on neuron like cells. Preliminary results show that TM cells are less sensitive to pressure elevation than OS, and OS-damaging effects were worsened by the pressure increase. The stressed TM releases harmful signals which increase apoptosis stimuli on neuron-like cells, suggesting its pivotal role in the glaucoma cascade.
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