Early postnatal Müller cell death leads to retinal but not optic nerve degeneration in NSE-Hu-Bcl-2 transgenic mice

Dubois‐Dauphin, Michel; Poitry-Yamate, C L; Bilbao, Fabienne de; Julliard, A; Jourdan, F; Donati, G.

doi:10.1016/s0306-4522(99)00313-9

Cited by 65 publications

(49 citation statements)

References 51 publications

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“…Thus, damage of the entire retina may occur. This conclusion may in agreement with the Mizutani et al report [36] , which stated that selective Müller cell functional abnormalities in early stage of the development of diabetic retinopathy, and with the report of Dubois et al [37] , who found Müller cells death causes retinal dysplasia, photoreceptor apopotosis, and finally retinal degeneration and proliferation of the retinal pigment epithelium. Another reason that reinforce the concept of retinal degeneration by sorbitol pathway is the protection or delaying of diabetic retinopathy by using aldose reductase inhibitor (tolrestat) in diabetic rats [14] , prevention of glomerular disease by aldose reductase inhibitor (sorbinil) in diabetic rats [38] , correcting corneal endothelial changes in diabetic patient by topical aldose reductase inhibitor (placebo) in diabetic patients [39] , Prevention of diabetic complications and nerve tissue by aldose reductase inhibitors (sorbinil or sulindac) in rats lens [40] , prevention of diabetic retinopathy by aldose reductase inhibitor (sorbinil) in diabetic patients [41] , and prevention of basement membrane thickening by aldose reductase inhibitor (sorbinil) in retina of galactosemic rats [3] .…”

Section: Discussionsupporting

confidence: 82%

Sorbitol-Induced Diabetic-Like Retinal Lesions in Rats: Microscopic Study

Ramadan¹

2007

American J. of Pharmacology and Toxicology

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Abstract:The present study investigated the sorbitol toxicity on the retinas of normal albino rats and founded by the light microscope that intra-peritoneal injection of Sorbitol (10-mg/kg-body weight per day) for 24 weeks produced similar diabetic like retinal lesions in these rats. The retinopathic effects of sorbitol injection affect retinal microvessels, pigment epithelium, neural retina and glial cells. Cytoplasmic vacuolation of the pigment epithelium and oedema of the neural retinal cells were evident. Microvascular abnormalities include thick-walled, elongated and dilated blood capillaries. The abnormal capillaries showed aneurysms and were occluded with deformed, fragmented, and adherent blood cells. Another finding was the pyknosis of glial cells. The present investigation concluded that sorbitol is toxic to the retinal tissue and it may play a role in the setup of diabetic retinopathy.

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Section: Discussionsupporting

confidence: 82%

Sorbitol-Induced Diabetic-Like Retinal Lesions in Rats: Microscopic Study

Ramadan¹

2007

American J. of Pharmacology and Toxicology

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“…Spanning the entire width of the retina, MG define the retinal boundaries through the formation of intercellular junctions, function as a neuronal scaffold, and play the decisive role in the establishment of retinal laminar pattern and polarity (Bringmann et al, 2006;Willbold et al, 1997). Consistent with this role, the loss of MG in the postnatal retina results in retinal degeneration (Dubois-Dauphin et al, 1999;Rich et al, 1995). In agreement with these observations, we find that the gradual loss of MG cells in Sox2…”

Section: Discussionsupporting

confidence: 80%

“…Mutations leading to a reduced density of MG or that alter their ability to function as a structural scaffold are associated with the disruption of the inner and outer retinal membranes and of neuronal stratification, eventually resulting in retinal degeneration (Dubois-Dauphin et al, 1999;van Rossum et al, 2006). The reduced density and aberrant localization of MG throughout the INL and ONL in SOX2-deficient retinas, combined with the disorganization of the ONL, led us to examine the laminar architecture in Sox2 MUTANT retinas.…”

Section: Aberrant Mg Morphology and Laminar Disorganization In Sox2mentioning

confidence: 99%

SOX2 maintains the quiescent progenitor cell state of postnatal retinal Müller glia

et al. 2013

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SUMMARYWithin discrete regions of the developing mammalian central nervous system, small subsets of glia become specialized to function as neural stem cells. As a result of their self-renewal and neurogenic capacity, these cells later serve to replenish neurons and glia during persistent or injury-induced adult neurogenesis. SOX2, an HMG box transcription factor, plays an essential role in the maintenance of both embryonic and adult neural progenitors. It is unclear, however, which biological mechanisms regulated by SOX2 are required for neural stem cell maintenance. In this study, we address this question through genetic analysis of SOX2 function in differentiating postnatal Müller glia, a cell type that maintains neurogenic capacity in the adult retina. By utilizing molecular analysis and real-time imaging, we show that two progenitor characteristics of nascent Müller glia -their radial morphology and cell cycle quiescence -are disrupted following conditional genetic ablation of Sox2 in the mouse postnatal retina, leading to Müller cell depletion and retinal degeneration. Moreover, we demonstrate that genetic induction of the Notch signaling pathway restores Müller glial cell identity to Sox2 mutant cells, but does not secure their quiescent state. Collectively, these results uncouple the roles of SOX2 and the Notch signaling pathway in the postnatal retina, and uncover a novel role for SOX2 in preventing the depletion of postnatal Müller glia through terminal cell division.

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“…Among these retinal cells, Müller glia are the only ones whose cell bodies span virtually the entire thickness of the retina from the outer nuclear layer (ONL) to the optic nerve fiber layer/inner limiting membrane layer (NFL/ILML), ensheathing every individual neuronal cell in the adult retina (1). Consistent with the structural relationships between Müller glia and other retinal cells, it is believed that Müller glia are critical for the survival and function of retinal neurons in both normal and pathogenic conditions, thus serving multiple functions carried out by astrocytes and oligodendrocytes in other parts of the central nervous system (1,5,13,36).…”

mentioning

confidence: 98%