Cell-Subtype-Specific Remodeling of Intrinsically Photosensitive Retinal Ganglion Cells in Streptozotocin-Induced Diabetic Mice

Diabetes ◽  
2021 ◽  
pp. db200775
Author(s):  
Wei-Yi Chen ◽  
Xu Han ◽  
Ling-Jie Cui ◽  
Chen-Xi Yu ◽  
Wen-Long Sheng ◽  
...  
Keyword(s):  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Retinal Ganglion ◽  
Diabetic Mice ◽  
Cell Subtype

scholarly journals Cell-Subtype-Specific Remodeling of Intrinsically Photosensitive Retinal Ganglion Cells in Streptozotocin-Induced Diabetic Mice

2021 ◽  
Author(s):  
Wei-Yi Chen ◽  
Xu Han ◽  
Ling-Jie Cui ◽  
Chen-Xi Yu ◽  
Wen-Long Sheng ◽  
...  
Keyword(s):  
Neurodegenerative Diseases ◽  
Retinal Ganglion Cells ◽  
Visual Function ◽  
Functional Activity ◽  
Ganglion Cells ◽  
Early Stage ◽  
Retinal Ganglion ◽  
Diabetic Mice ◽  
Pupillary Light ◽  
Dendritic Branching

Recent evidence suggests that melanopsin-expressing intrinsically photosensitive retinal ganglion cells (ipRGCs), a neuronal class regulating non-image forming (NIF) vision and generally thought to be injury-resistant, are dysfunctional in certain neurodegenerative diseases. Although disrupted NIF visual functions have been reported in patients and animals with diabetes, it remains controversial whether ipRGCs exhibit remodeling during diabetes and if so, whether such remodeling is variable among ipRGC subtypes. Here we demonstrate that survival, soma-dendritic profiles and melanopsin-based functional activity of M1 ipRGCs were unaltered in streptozotocin-induced 3-month diabetic mice. Such resistance remained at 6 months after streptozotocin administration. In contrast, M2/M3 ipRGCs underwent significant remodeling in diabetic mice, manifested by enlarged somata and increased dendritic branching complexity. Consistent with the unaltered melanopsin levels, the sensitivity of melanopsin-based activity was unchanged in surviving M2 cells, but their response gain displayed a compensatory enhancement. Meanwhile, the pupillary light reflex, a NIF visual function controlled by M2 cells, was found to be impaired in diabetic animals. The resistance of M1 cells might be attributed to the adjacency of their dendrites to capillaries, which makes them less disturbed by the impaired retinal blood supply at the early stage of diabetes.

Analysis of sigma receptor (σR1) expression in retinal ganglion cells cultured under hyperglycemic conditions and in diabetic mice

2002 ◽  
Vol 107 (2) ◽  
pp. 97-107 ◽  
Author(s):  
M Shamsul Ola ◽  
Pamela Moore ◽  
Dennis Maddox ◽  
Amira El-Sherbeny ◽  
Wei Huang ◽  
...  
Keyword(s):  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Sigma Receptor ◽  
Retinal Ganglion ◽  
Diabetic Mice ◽  
Cells Cultured

scholarly journals Hyperactivity of ON-Type Retinal Ganglion Cells in Streptozotocin-Induced Diabetic Mice

PLoS ONE ◽  
2013 ◽  
Vol 8 (9) ◽  
pp. e76049 ◽  
Author(s):  
Jun Yu ◽  
Lu Wang ◽  
Shi-Jun Weng ◽  
Xiong-Li Yang ◽  
Dao-Qi Zhang ◽  
...  
Keyword(s):  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Retinal Ganglion ◽  
Diabetic Mice

scholarly journals Cell-Subtype-Specific Remodeling of Intrinsically Photosensitive Retinal Ganglion Cells in Streptozotocin-Induced Diabetic Mice

2021 ◽  
Author(s):  
Wei-Yi Chen ◽  
Xu Han ◽  
Ling-Jie Cui ◽  
Chen-Xi Yu ◽  
Wen-Long Sheng ◽  
...  
Keyword(s):  
Neurodegenerative Diseases ◽  
Retinal Ganglion Cells ◽  
Visual Function ◽  
Functional Activity ◽  
Ganglion Cells ◽  
Early Stage ◽  
Retinal Ganglion ◽  
Diabetic Mice ◽  
Pupillary Light ◽  
Dendritic Branching

Recent evidence suggests that melanopsin-expressing intrinsically photosensitive retinal ganglion cells (ipRGCs), a neuronal class regulating non-image forming (NIF) vision and generally thought to be injury-resistant, are dysfunctional in certain neurodegenerative diseases. Although disrupted NIF visual functions have been reported in patients and animals with diabetes, it remains controversial whether ipRGCs exhibit remodeling during diabetes and if so, whether such remodeling is variable among ipRGC subtypes. Here we demonstrate that survival, soma-dendritic profiles and melanopsin-based functional activity of M1 ipRGCs were unaltered in streptozotocin-induced 3-month diabetic mice. Such resistance remained at 6 months after streptozotocin administration. In contrast, M2/M3 ipRGCs underwent significant remodeling in diabetic mice, manifested by enlarged somata and increased dendritic branching complexity. Consistent with the unaltered melanopsin levels, the sensitivity of melanopsin-based activity was unchanged in surviving M2 cells, but their response gain displayed a compensatory enhancement. Meanwhile, the pupillary light reflex, a NIF visual function controlled by M2 cells, was found to be impaired in diabetic animals. The resistance of M1 cells might be attributed to the adjacency of their dendrites to capillaries, which makes them less disturbed by the impaired retinal blood supply at the early stage of diabetes.

scholarly journals IL-17A injury to retinal ganglion cells is mediated by retinal Müller cells in diabetic retinopathy

2021 ◽  
Vol 12 (11) ◽  
Author(s):  
Ao-Wang Qiu ◽  
Da-Rui Huang ◽  
Bin Li ◽  
Yuan Fang ◽  
Wei-Wei Zhang ◽  
...  
Keyword(s):  
Diabetic Retinopathy ◽  
T Lymphocytes ◽  
Retinal Ganglion Cells ◽  
Neuronal Death ◽  
Ganglion Cells ◽  
Müller Cells ◽  
Retinal Ganglion ◽  
Muller Cells ◽  
Diabetic Mice

AbstractDiabetic retinopathy (DR), the most common and serious ocular complication, recently has been perceived as a neurovascular inflammatory disease. However, role of adaptive immune inflammation driven by T lymphocytes in DR is not yet well elucidated. Therefore, this study aimed to clarify the role of interleukin (IL)-17A, a proinflammatory cytokine mainly produced by T lymphocytes, in retinal pathophysiology particularly in retinal neuronal death during DR process. Ins2Akita (Akita) diabetic mice 12 weeks after the onset of diabetes were used as a DR model. IL-17A-deficient diabetic mice were obtained by hybridization of IL-17A-knockout (IL-17A-KO) mouse with Akita mouse. Primarily cultured retinal Müller cells (RMCs) and retinal ganglion cells (RGCs) were treated with IL-17A in high-glucose (HG) condition. A transwell coculture of RGCs and RMCs whose IL-17 receptor A (IL-17RA) gene had been silenced with IL-17RA-shRNA was exposed to IL-17A in HG condition and the cocultured RGCs were assessed on their survival. Diabetic mice manifested increased retinal microvascular lesions, RMC activation and dysfunction, as well as RGC apoptosis. IL-17A-KO diabetic mice showed reduced retinal microvascular impairments, RMC abnormalities, and RGC apoptosis compared with diabetic mice. RMCs expressed IL-17RA. IL-17A exacerbated HG-induced RMC activation and dysfunction in vitro and silencing IL-17RA gene in RMCs abolished the IL-17A deleterious effects. In contrast, RGCs did not express IL-17RA and IL-17A did not further alter HG-induced RGC death. Notably, IL-17A aggravated HG-induced RGC death in the presence of intact RMCs but not in the presence of RMCs in which IL-17RA gene had been knocked down. These findings establish that IL-17A is actively involved in DR pathophysiology and particularly by RMC mediation it promotes RGC death. Collectively, we propose that antagonizing IL-17RA on RMCs may prevent retinal neuronal death and thereby slow down DR progression.

scholarly journals ON-Type Retinal Ganglion Cells are Preferentially Affected in STZ-Induced Diabetic Mice

2019 ◽  
Vol 60 (5) ◽  
pp. 1644 ◽  
Author(s):  
Run-Ze Cui ◽  
Lu Wang ◽  
Sheng-Nan Qiao ◽  
Yong-Chen Wang ◽  
Xin Wang ◽  
...  
Keyword(s):  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Retinal Ganglion ◽  
Diabetic Mice

scholarly journals Cell-Subtype-Specific Remodeling of Intrinsically Photosensitive Retinal Ganglion Cells in Streptozotocin-Induced Diabetic Mice

2021 ◽  
Author(s):  
Ada Admin ◽  
Wei-Yi Chen ◽  
Xu Han ◽  
Ling-Jie Cui ◽  
Chen-Xi Yu ◽  
...  
Keyword(s):  
Neurodegenerative Diseases ◽  
Retinal Ganglion Cells ◽  
Visual Function ◽  
Functional Activity ◽  
Ganglion Cells ◽  
Early Stage ◽  
Retinal Ganglion ◽  
Diabetic Mice ◽  
Pupillary Light ◽  
Dendritic Branching

Recent evidence suggests that melanopsin-expressing intrinsically photosensitive retinal ganglion cells (ipRGCs), a neuronal class regulating non-image forming (NIF) vision and generally thought to be injury-resistant, are dysfunctional in certain neurodegenerative diseases. Although disrupted NIF visual functions have been reported in patients and animals with diabetes, it remains controversial whether ipRGCs exhibit remodeling during diabetes and if so, whether such remodeling is variable among ipRGC subtypes. Here we demonstrate that survival, soma-dendritic profiles and melanopsin-based functional activity of M1 ipRGCs were unaltered in streptozotocin-induced 3-month diabetic mice. Such resistance remained at 6 months after streptozotocin administration. In contrast, M2/M3 ipRGCs underwent significant remodeling in diabetic mice, manifested by enlarged somata and increased dendritic branching complexity. Consistent with the unaltered melanopsin levels, the sensitivity of melanopsin-based activity was unchanged in surviving M2 cells, but their response gain displayed a compensatory enhancement. Meanwhile, the pupillary light reflex, a NIF visual function controlled by M2 cells, was found to be impaired in diabetic animals. The resistance of M1 cells might be attributed to the adjacency of their dendrites to capillaries, which makes them less disturbed by the impaired retinal blood supply at the early stage of diabetes.

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