Potential of Müller Glia for Retina Neuroprotection

Eastlake, Karen; Luis, Joshua; Limb, G. Astrid

doi:10.1080/02713683.2019.1648831

Cited by 43 publications

(39 citation statements)

References 93 publications

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“…Previous studies indicated that neurotoxic stimuli and glial cell secretion activated the production of not only proin ammatory cytokines but also growth factors in Müller and microglial cells 25,[34][35][36][37] .…”

Section: Discussionmentioning

confidence: 99%

Glial Cells Modulate Retinal Cell Survival in Rotenone-Induced Neural Degeneration

Tawarayama

Inoue-Yanagimachi

Himori

et al. 2021

Preprint

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Administration of the mitochondrial complex I inhibitor rotenone provides an excellent model to study the pathomechanism of oxidative stress-related neural degeneration diseases. In this study, we examined the glial roles in retinal cell survival and degeneration under the rotenone-induced oxidative stress condition. Mouse-derived Müller, microglial (BV-2), and dissociated retinal cells were used for in vitro experiments. Gene expression levels and cell viability were determined using quantitative reverse transcription-polymerase chain reaction and the alamarBlue assay, respectively. Conditioned media were prepared by stimulating glial cells with rotenone. Retinal ganglion cells (RGCs) and inner nuclear layer (INL) were visualized on rat retinal sections by immunohistochemistry and eosin/hematoxylin, respectively. Rotenone dose-dependently induced glial cell death. Treatment with rotenone or rotenone-stimulated glial cell-conditioned media altered gene expression of growth factors and inflammatory cytokines in glial cells. The viability of dissociated retinal cells significantly increased upon culturing in media conditioned with rotenone-stimulated or Müller cell-conditioned media-stimulated BV-2 cells. Furthermore, intravitreal neurotrophin-5 administration prevented the rotenone-induced reduction of RGC number and INL thickness in rats. Thus, glial cells exerted both positive and negative effects on retinal cell survival in rotenone-induced neural degeneration via altered expression of growth factors, especially upregulation of microglia-derived Ntf5, and proinflammatory cytokines.

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Section: Discussionmentioning

confidence: 99%

Glial Cells Modulate Retinal Cell Survival in Rotenone-Induced Neural Degeneration

Tawarayama

Inoue-Yanagimachi

Himori

et al. 2021

Preprint

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“…This may explain the fact that retinal damages and visual impairments occurred during the high dose melatonin administration. Müller cells constitute the main glial cells of the retina (Eastlake et al., 2020 ). They are spatially distributed across retinal laminations, facilitating their close membrane interactions with different types of retinal neurons (Di Pierdomenico et al., 2020 ).…”

Section: Discussionmentioning

confidence: 99%

Intravitreous delivery of melatonin affects the retinal neuron survival and visual signal transmission: in vivo and ex vivo study

Tao

et al. 2020

Drug Delivery

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Intravitreal delivery can maximize the intensity of therapeutic agents and extend their residence time within ocular tissue. Melatonin is a lipophilic molecule that crosses freely biological barriers and cell membranes. This study intends to investigate the effects of intravitreally delivered melatonin on mouse retina. The visual function of administered mice is assessed by electrophysiological and behavior examinations three weeks after intravitreal delivery. Moreover, multi-electrode array (MEA) was used to assess the electrical activities of retinal ganglion cells (RGCs). We found that intravitreal delivery of high dosage melatonin (400–500 µg/kg) destroyed the retinal architecture and impaired the visual function of mice. Conversely, the melatonin administration at low dose (100–300 µg/kg) did not have any significant effects on the photoreceptor survival or visual function. As shown in the MEA recording, the photoreceptors activity of the central region was more severely disturbed by the high dose melatonin. A pronounced augment of the spontaneous firing frequency was recorded in these mice received high dosage melatonin, indicating that intravitreal delivery of high dosage melatonin would affect the electrical activity of RGCs. Immunostaining assay showed that the vitality of cone photoreceptor was impaired by high dose melatonin. These findings suggest that intravitreal melatonin is not always beneficial for ocular tissues, especially when it is administered at high dosage. These data add new perspectives to current knowledge about melatonin delivery at the ocular level. Further therapeutic strategies should take into consideration of these risks that caused by delivery approach.

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“…In addition, due to their energy metabolism, Müller cells may protect neurons towards toxic stress by increasing ATP turnover [263]. Furthermore, they play a role in water and ion regulation, buffering the retina and inducing neuroprotection [250,264]. It is worth highlighting the important antioxidant role of Müller cells.…”

Section: Glia-mediated Neuroprotectionmentioning

confidence: 99%

Neuroprotective Strategies for Retinal Ganglion Cell Degeneration: Current Status and Challenges Ahead

Boia

Ruzafa

Aires

et al. 2020

IJMS

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The retinal ganglion cells (RGCs) are the output cells of the retina into the brain. In mammals, these cells are not able to regenerate their axons after optic nerve injury, leaving the patients with optic neuropathies with permanent visual loss. An effective RGCs-directed therapy could provide a beneficial effect to prevent the progression of the disease. Axonal injury leads to the functional loss of RGCs and subsequently induces neuronal death, and axonal regeneration would be essential to restore the neuronal connectivity, and to reestablish the function of the visual system. The manipulation of several intrinsic and extrinsic factors has been proposed in order to stimulate axonal regeneration and functional repairing of axonal connections in the visual pathway. However, there is a missing point in the process since, until now, there is no therapeutic strategy directed to promote axonal regeneration of RGCs as a therapeutic approach for optic neuropathies.

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Potential of Müller Glia for Retina Neuroprotection

Cited by 43 publications

References 93 publications

Glial Cells Modulate Retinal Cell Survival in Rotenone-Induced Neural Degeneration

Glial Cells Modulate Retinal Cell Survival in Rotenone-Induced Neural Degeneration

Intravitreous delivery of melatonin affects the retinal neuron survival and visual signal transmission: in vivo and ex vivo study

Neuroprotective Strategies for Retinal Ganglion Cell Degeneration: Current Status and Challenges Ahead

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