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Diabetes Exacerbates the Intraocular Pressure-Independent Retinal Ganglion Cells Degeneration in the DBA/2J Model of Glaucoma.
Invest Ophthalmol Vis Sci. 2021 07 01; 62(9):9.IO

Abstract

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.

Authors+Show Affiliations

Department of Biology, University of Pisa, Pisa, Italy. Bascom Palmer Eye Institute, Miller School of Medicine, University of Miami, Miami, Florida, United States.Bascom Palmer Eye Institute, Miller School of Medicine, University of Miami, Miami, Florida, United States. Biomedical and Biotechnological Sciences Department, University of Catania, Catania, Italy.Bascom Palmer Eye Institute, Miller School of Medicine, University of Miami, Miami, Florida, United States.Bascom Palmer Eye Institute, Miller School of Medicine, University of Miami, Miami, Florida, United States. Biomedical and Biotechnological Sciences Department, University of Catania, Catania, Italy.Department of Biology, University of Pisa, Pisa, Italy.Department of Biology, University of Pisa, Pisa, Italy.Department of Biology, University of Pisa, Pisa, Italy.Bascom Palmer Eye Institute, Miller School of Medicine, University of Miami, Miami, Florida, United States.

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

34232257

Citation

Amato, Rosario, et al. "Diabetes Exacerbates the Intraocular Pressure-Independent Retinal Ganglion Cells Degeneration in the DBA/2J Model of Glaucoma." Investigative Ophthalmology & Visual Science, vol. 62, no. 9, 2021, p. 9.
Amato R, Lazzara F, Chou TH, et al. Diabetes Exacerbates the Intraocular Pressure-Independent Retinal Ganglion Cells Degeneration in the DBA/2J Model of Glaucoma. Invest Ophthalmol Vis Sci. 2021;62(9):9.
Amato, R., Lazzara, F., Chou, T. H., Romano, G. L., Cammalleri, M., Dal Monte, M., Casini, G., & Porciatti, V. (2021). Diabetes Exacerbates the Intraocular Pressure-Independent Retinal Ganglion Cells Degeneration in the DBA/2J Model of Glaucoma. Investigative Ophthalmology & Visual Science, 62(9), 9. https://doi.org/10.1167/iovs.62.9.9
Amato R, et al. Diabetes Exacerbates the Intraocular Pressure-Independent Retinal Ganglion Cells Degeneration in the DBA/2J Model of Glaucoma. Invest Ophthalmol Vis Sci. 2021 07 1;62(9):9. PubMed PMID: 34232257.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Diabetes Exacerbates the Intraocular Pressure-Independent Retinal Ganglion Cells Degeneration in the DBA/2J Model of Glaucoma. AU - Amato,Rosario, AU - Lazzara,Francesca, AU - Chou,Tsung-Han, AU - Romano,Giovanni Luca, AU - Cammalleri,Maurizio, AU - Dal Monte,Massimo, AU - Casini,Giovanni, AU - Porciatti,Vittorio, PY - 2021/7/7/entrez PY - 2021/7/8/pubmed PY - 2021/10/5/medline SP - 9 EP - 9 JF - Investigative ophthalmology & visual science JO - Invest Ophthalmol Vis Sci VL - 62 IS - 9 N2 - 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. SN - 1552-5783 UR - https://www.unboundmedicine.com/medline/citation/34232257/Diabetes_Exacerbates_the_Intraocular_Pressure_Independent_Retinal_Ganglion_Cells_Degeneration_in_the_DBA/2J_Model_of_Glaucoma_ L2 - https://iovs.arvojournals.org/article.aspx?doi=10.1167/iovs.62.9.9 DB - PRIME DP - Unbound Medicine ER -