2017
DOI: 10.1002/glia.23243
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Microglial‐induced Müller cell gliosis is attenuated by progesterone in a mouse model of retinitis pigmentosa

Abstract: Norgestrel, a progesterone analogue, has demonstrated neuroprotective effects in a mouse model of retinitis pigmentosa. Neuroprotection is achieved in part through Norgestrels anti-inflammatory properties, alleviating detrimental microglial activity. Gliosis is a feature of many neurodegenerative diseases of the retina, including retinitis pigmentosa. Müller glia, a type of macroglia found in the retina, are major contributors of gliosis, characterized by the upregulation of glial fibrillary acidic protein (GF… Show more

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Cited by 57 publications
(58 citation statements)
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“…Other authors have also found migration of microglia and macrophages to the outer retina in other models of light-induced retinal degeneration 59,110 and activated microglial cells at the center of the rings of photoreceptor degeneration in a rat model of inherited retinal degeneration, before the occupation of the rings by processes of Müller cells. 29 Microglial cells and Müller cells might act coordinately to phagocytose photoreceptor debris during retinal degeneration 48,49,60,111,112 ; Müller cells may release factors that induce microglial activation and migration, 96,100,103 and may also form a scaffold to guide microglial migration, 49,60 whereas activated microglia may also release factors that influence Müller cells behavior. 111,113 Specifically, microglial activation may influence the morphology and function of Müller cells, stimulating Müller cell gliosis but a decrease of their phagocytic activity.…”
Section: Figurementioning
confidence: 99%
See 1 more Smart Citation
“…Other authors have also found migration of microglia and macrophages to the outer retina in other models of light-induced retinal degeneration 59,110 and activated microglial cells at the center of the rings of photoreceptor degeneration in a rat model of inherited retinal degeneration, before the occupation of the rings by processes of Müller cells. 29 Microglial cells and Müller cells might act coordinately to phagocytose photoreceptor debris during retinal degeneration 48,49,60,111,112 ; Müller cells may release factors that induce microglial activation and migration, 96,100,103 and may also form a scaffold to guide microglial migration, 49,60 whereas activated microglia may also release factors that influence Müller cells behavior. 111,113 Specifically, microglial activation may influence the morphology and function of Müller cells, stimulating Müller cell gliosis but a decrease of their phagocytic activity.…”
Section: Figurementioning
confidence: 99%
“…29 Microglial cells and Müller cells might act coordinately to phagocytose photoreceptor debris during retinal degeneration 48,49,60,111,112 ; Müller cells may release factors that induce microglial activation and migration, 96,100,103 and may also form a scaffold to guide microglial migration, 49,60 whereas activated microglia may also release factors that influence Müller cells behavior. 111,113 Specifically, microglial activation may influence the morphology and function of Müller cells, stimulating Müller cell gliosis but a decrease of their phagocytic activity. 49,60,114 We also show in this study that 2 or 3 months ALE, the microglial cells disappear from the center of the rings and concentrate in their periphery and, when all the cones disappear, the microglial cells resume their normal homogeneous distribution within the areas devoid of cones.…”
Section: Figurementioning
confidence: 99%
“…Immediately after injury, Müller cells generate neurotrophic factors to promote recovery (Garcia and Vecino 2003;Bringmann et al 2006Bringmann et al , 2009b. However, chronic gliosis contributes to degeneration and impedes tissue regeneration (Roche et al 2018). Currently, the molecular and cellular requirements necessary for the successful regeneration of different organs in mammals and teleost are not well known.…”
Section: Introductionmentioning
confidence: 99%
“…Furthermore, SIS3 treatment reveals the possible communication between TGFβ1/2 with Notch1/2 and their combined action might promote the transition from a mesenchymal to an epithelial phenotype in mammalian MCs (MC-ET) after injury. Thus, Smad3 seems a promising target to improve the detrimental effects of chronic reactive gliosis, such as glial scar formation known as a physical barrier of retinal regeneration in mammals [56].…”
Section: Discussionmentioning
confidence: 99%