An Innovative In Vitro Open-Angle Glaucoma Model (IVOM) Shows Changes Induced by Increased Ocular Pressure and Oxidative Stress

Primary Open-Angle Glaucoma (POAG) is a neurodegenerative disease, and its clinical outcomes lead to visual field constriction and blindness. POAG’s etiology is very complex and its pathogenesis is mainly explained through both mechanical and vascular theories. The trabecular meshwork (TM), the most...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: Stefania Vernazza, Sara Tirendi, Mario Passalacqua, Francesco Piacente, Sonia Scarfì, Francesco Oddone, Anna Maria Bassi
Formato: article
Lenguaje:EN
Publicado: MDPI AG 2021
Materias:
Acceso en línea:https://doaj.org/article/f340dc1b1f00484c8e015951ea5f2fa0
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
id oai:doaj.org-article:f340dc1b1f00484c8e015951ea5f2fa0
record_format dspace
spelling oai:doaj.org-article:f340dc1b1f00484c8e015951ea5f2fa02021-11-25T17:53:37ZAn Innovative In Vitro Open-Angle Glaucoma Model (IVOM) Shows Changes Induced by Increased Ocular Pressure and Oxidative Stress10.3390/ijms2222121291422-00671661-6596https://doaj.org/article/f340dc1b1f00484c8e015951ea5f2fa02021-11-01T00:00:00Zhttps://www.mdpi.com/1422-0067/22/22/12129https://doaj.org/toc/1661-6596https://doaj.org/toc/1422-0067Primary Open-Angle Glaucoma (POAG) is a neurodegenerative disease, and its clinical outcomes lead to visual field constriction and blindness. POAG’s 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. Preclinical assessments of neuroprotective drugs on animal models have not always shown correspondence with human clinical studies. In addition, intra-ocular pressure management after a glaucoma diagnosis does not always prevent blindness. Recently, we have been developing an innovative in vitro 3Dadvanced human trabecular cell model on a millifluidicplatform as a tool to improve glaucoma studies. Herein, we analyze the effects of prolonged increased pressure alone and, in association with OS, on such in vitro platform. Moreover, we verify whethersuch damaged TM triggers apoptosis on neuron-like cells. The 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.Stefania VernazzaSara TirendiMario PassalacquaFrancesco PiacenteSonia ScarfìFrancesco OddoneAnna Maria BassiMDPI AGarticle3D modelglaucomatrabecular meshworkbioreactorBiology (General)QH301-705.5ChemistryQD1-999ENInternational Journal of Molecular Sciences, Vol 22, Iss 12129, p 12129 (2021)
institution DOAJ
collection DOAJ
language EN
topic 3D model
glaucoma
trabecular meshwork
bioreactor
Biology (General)
QH301-705.5
Chemistry
QD1-999
spellingShingle 3D model
glaucoma
trabecular meshwork
bioreactor
Biology (General)
QH301-705.5
Chemistry
QD1-999
Stefania Vernazza
Sara Tirendi
Mario Passalacqua
Francesco Piacente
Sonia Scarfì
Francesco Oddone
Anna Maria Bassi
An Innovative In Vitro Open-Angle Glaucoma Model (IVOM) Shows Changes Induced by Increased Ocular Pressure and Oxidative Stress
description Primary Open-Angle Glaucoma (POAG) is a neurodegenerative disease, and its clinical outcomes lead to visual field constriction and blindness. POAG’s 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. Preclinical assessments of neuroprotective drugs on animal models have not always shown correspondence with human clinical studies. In addition, intra-ocular pressure management after a glaucoma diagnosis does not always prevent blindness. Recently, we have been developing an innovative in vitro 3Dadvanced human trabecular cell model on a millifluidicplatform as a tool to improve glaucoma studies. Herein, we analyze the effects of prolonged increased pressure alone and, in association with OS, on such in vitro platform. Moreover, we verify whethersuch damaged TM triggers apoptosis on neuron-like cells. The 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.
format article
author Stefania Vernazza
Sara Tirendi
Mario Passalacqua
Francesco Piacente
Sonia Scarfì
Francesco Oddone
Anna Maria Bassi
author_facet Stefania Vernazza
Sara Tirendi
Mario Passalacqua
Francesco Piacente
Sonia Scarfì
Francesco Oddone
Anna Maria Bassi
author_sort Stefania Vernazza
title An Innovative In Vitro Open-Angle Glaucoma Model (IVOM) Shows Changes Induced by Increased Ocular Pressure and Oxidative Stress
title_short An Innovative In Vitro Open-Angle Glaucoma Model (IVOM) Shows Changes Induced by Increased Ocular Pressure and Oxidative Stress
title_full An Innovative In Vitro Open-Angle Glaucoma Model (IVOM) Shows Changes Induced by Increased Ocular Pressure and Oxidative Stress
title_fullStr An Innovative In Vitro Open-Angle Glaucoma Model (IVOM) Shows Changes Induced by Increased Ocular Pressure and Oxidative Stress
title_full_unstemmed An Innovative In Vitro Open-Angle Glaucoma Model (IVOM) Shows Changes Induced by Increased Ocular Pressure and Oxidative Stress
title_sort innovative in vitro open-angle glaucoma model (ivom) shows changes induced by increased ocular pressure and oxidative stress
publisher MDPI AG
publishDate 2021
url https://doaj.org/article/f340dc1b1f00484c8e015951ea5f2fa0
work_keys_str_mv AT stefaniavernazza aninnovativeinvitroopenangleglaucomamodelivomshowschangesinducedbyincreasedocularpressureandoxidativestress
AT saratirendi aninnovativeinvitroopenangleglaucomamodelivomshowschangesinducedbyincreasedocularpressureandoxidativestress
AT mariopassalacqua aninnovativeinvitroopenangleglaucomamodelivomshowschangesinducedbyincreasedocularpressureandoxidativestress
AT francescopiacente aninnovativeinvitroopenangleglaucomamodelivomshowschangesinducedbyincreasedocularpressureandoxidativestress
AT soniascarfi aninnovativeinvitroopenangleglaucomamodelivomshowschangesinducedbyincreasedocularpressureandoxidativestress
AT francescooddone aninnovativeinvitroopenangleglaucomamodelivomshowschangesinducedbyincreasedocularpressureandoxidativestress
AT annamariabassi aninnovativeinvitroopenangleglaucomamodelivomshowschangesinducedbyincreasedocularpressureandoxidativestress
AT stefaniavernazza innovativeinvitroopenangleglaucomamodelivomshowschangesinducedbyincreasedocularpressureandoxidativestress
AT saratirendi innovativeinvitroopenangleglaucomamodelivomshowschangesinducedbyincreasedocularpressureandoxidativestress
AT mariopassalacqua innovativeinvitroopenangleglaucomamodelivomshowschangesinducedbyincreasedocularpressureandoxidativestress
AT francescopiacente innovativeinvitroopenangleglaucomamodelivomshowschangesinducedbyincreasedocularpressureandoxidativestress
AT soniascarfi innovativeinvitroopenangleglaucomamodelivomshowschangesinducedbyincreasedocularpressureandoxidativestress
AT francescooddone innovativeinvitroopenangleglaucomamodelivomshowschangesinducedbyincreasedocularpressureandoxidativestress
AT annamariabassi innovativeinvitroopenangleglaucomamodelivomshowschangesinducedbyincreasedocularpressureandoxidativestress
_version_ 1718411898667401216