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Diabetes Exacerbates the Intraocular Pressure-Independent Retinal Ganglion Cells Degeneration in the DBA/2J Model of Glaucoma.
Amato, Rosario; Lazzara, Francesca; Chou, Tsung-Han; Romano, Giovanni Luca; Cammalleri, Maurizio; Dal Monte, Massimo; Casini, Giovanni; Porciatti, Vittorio.
Afiliação
  • Amato R; Department of Biology, University of Pisa, Pisa, Italy.
  • Lazzara F; Bascom Palmer Eye Institute, Miller School of Medicine, University of Miami, Miami, Florida, United States.
  • Chou TH; Bascom Palmer Eye Institute, Miller School of Medicine, University of Miami, Miami, Florida, United States.
  • Romano GL; Biomedical and Biotechnological Sciences Department, University of Catania, Catania, Italy.
  • Cammalleri M; Bascom Palmer Eye Institute, Miller School of Medicine, University of Miami, Miami, Florida, United States.
  • Dal Monte M; Bascom Palmer Eye Institute, Miller School of Medicine, University of Miami, Miami, Florida, United States.
  • Casini G; Biomedical and Biotechnological Sciences Department, University of Catania, Catania, Italy.
  • Porciatti V; Department of Biology, University of Pisa, Pisa, Italy.
Invest Ophthalmol Vis Sci ; 62(9): 9, 2021 07 01.
Article em En | MEDLINE | ID: mdl-34232257
Purpose: Glaucoma is a multifactorial disease, causing retinal ganglion cells (RGCs) and optic nerve degeneration. The role of diabetes as a risk factor for glaucoma has been postulated but still not unequivocally demonstrated. The purpose of this study is to clarify the effect of diabetes in the early progression of glaucomatous RGC dysfunction preceding intraocular pressure (IOP) elevation, using the DBA/2J mouse (D2) model of glaucoma. Methods: D2 mice were injected with streptozotocin (STZ) obtaining a combined model of diabetes and glaucoma (D2 + STZ). D2 and D2 + STZ mice were monitored for weight, glycemia, and IOP from 3.5 to 6 months of age. In addition, the activity of RGC and outer retina were assessed using pattern electroretinogram (PERG) and flash electroretinogram (FERG), respectively. At the end point, RGC density and astrogliosis were evaluated in flat mounted retinas. In addition, Müller cell reactivity was evaluated in retinal cross-sections. Finally, the expression of inflammation and oxidative stress markers were analyzed. Results: IOP was not influenced by time or diabetes. In contrast, RGC activity resulted progressively decreased in the D2 group independently from IOP elevation and outer retinal dysfunction. Diabetes exacerbated RGC dysfunction, which resulted independent from variation in IOP and outer retinal activity. Diabetic retinas displayed decreased RGC density and increased glial reactivity given by an increment in oxidative stress and inflammation. Conclusions: Diabetes can act as an IOP-independent risk factor for the early progression of glaucoma promoting oxidative stress and inflammation-mediated RGC dysfunction, glial reactivity, and cellular death.
Assuntos

Texto completo: 1 Coleções: 01-internacional Contexto em Saúde: 6_ODS3_enfermedades_notrasmisibles Base de dados: MEDLINE Assunto principal: Retina / Células Ganglionares da Retina / Glaucoma / Diabetes Mellitus Experimental / Pressão Intraocular Tipo de estudo: Diagnostic_studies / Etiology_studies / Prognostic_studies / Risk_factors_studies Limite: Animals Idioma: En Revista: Invest Ophthalmol Vis Sci Ano de publicação: 2021 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Contexto em Saúde: 6_ODS3_enfermedades_notrasmisibles Base de dados: MEDLINE Assunto principal: Retina / Células Ganglionares da Retina / Glaucoma / Diabetes Mellitus Experimental / Pressão Intraocular Tipo de estudo: Diagnostic_studies / Etiology_studies / Prognostic_studies / Risk_factors_studies Limite: Animals Idioma: En Revista: Invest Ophthalmol Vis Sci Ano de publicação: 2021 Tipo de documento: Article