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Understanding the Molecular Mechanisms of Retinal Ganglion Cell Death after Optic Nerve Damage

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (28 February 2022) | Viewed by 17567

Special Issue Editor

Dr. Takuji Kurimoto

E-Mail
Guest Editor
Division of Ophthalmology, Department of Surgery, Kobe University Graduate School of Medicine, Kobe, Japan
Interests: neuroprotection; retinal ganglion cells; axonal injury; neuronal cell death

Special Issue Information

Dear Colleagues,

The optic nerve is a bundle of axons from retinal ganglion cells (RGCs). Once it is injured, retrograde axonal degeneration occurs, and RGCs finally fall into cell death. Clinically, most optic neuropathies are still resistant to treatments, and beneficial regimens have yet to be established. A variety of animal models, including glaucoma, traumatic optic neuropathy, ischemic optic neuropathy, experimental autoimmune encephalomyelitis, etc., has been applied to elucidate pathological mechanisms. Notably, it has been suggested that RGC death is linked to inflammatory reaction, autophagy, oxidative reaction, mitochondrial dysfunction, and glucose and lactate metabolisms. This Special Issue explores recent advances in order to understand molecular mechanisms of RGC death better and solicits novel perspectives by expert review.

Dr. Takuji Kurimoto
Guest Editor

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Keywords

  • Autophagy
  • Mitochondrial dysfunction
  • inflammatory reaction
  • optic nerve crush/transection
  • glaucoma model
  • ischemic optic neuropathy model
  • Leber hereditary optic neuropathy model
  • glucose metabolism

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Published Papers (4 papers)

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Research

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15 pages, 5840 KiB  
Article
The Protective Effects of n-Butylidenephthalide on Retinal Ganglion Cells during Ischemic Injury
by Yu-Yau Chou, Jia-Ying Chien, Jhih-Wei Ciou and Shun-Ping Huang
Int. J. Mol. Sci. 2022, 23(4), 2095; https://doi.org/10.3390/ijms23042095 - 14 Feb 2022
Cited by 6 | Viewed by 2710
Abstract
Clinically, acute ischemic symptoms in the eyes are one of the main causes of vision loss, with the associated inflammatory response and oxidative stress being the key factors that cause injury. Nonarteritic anterior ischemic optic neuropathy (NAION) is the most common type of [...] Read more.
Clinically, acute ischemic symptoms in the eyes are one of the main causes of vision loss, with the associated inflammatory response and oxidative stress being the key factors that cause injury. Nonarteritic anterior ischemic optic neuropathy (NAION) is the most common type of ischemic optic neuropathy (ION); however, there are still no effective or safe treatment options to date. In this study, we investigated the neuroprotective effects of n-butylidenephthalide (BP) treatment in an experimental NAION rodent model (rAION). BP (10 mg/kg) or PBS (control group) were administered on seven consecutive days in the rAION model. Rats were evaluated for visual function by flash visual evoked potentials (FVEPs) at 4 weeks after NAION induction. The retina and optic nerve were removed for histological examination after the rats were euthanized. The molecular machinery of BP treatment in the rAION model was analyzed using Western blotting. We discovered that BP effectively improves retinal ganglion cell survival rates by preventing apoptotic processes after AION induction and reducing the inflammatory response through which blood-borne macrophages infiltrate the optic nerve. In addition, BP significantly preserved the integrity of the myelin sheath in the rAION model, demonstrating that BP can prevent the development of demyelination. Our immunoblotting results revealed the molecular mechanism through which BP mitigates the neuroinflammatory response through inhibition of the NF-κB signaling pathway. Taken together, these results demonstrate that BP can be used as an exceptional neuroprotective agent for ischemic injury. Full article
(This article belongs to the Special Issue Understanding the Molecular Mechanisms of Retinal Ganglion Cell Death after Optic Nerve Damage)
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18 pages, 2497 KiB  
Article
SARM1 Ablation Is Protective and Preserves Spatial Vision in an In Vivo Mouse Model of Retinal Ganglion Cell Degeneration
by Laura K. Finnegan, Naomi Chadderton, Paul F. Kenna, Arpad Palfi, Michael Carty, Andrew G. Bowie, Sophia Millington-Ward and G. Jane Farrar
Int. J. Mol. Sci. 2022, 23(3), 1606; https://doi.org/10.3390/ijms23031606 - 30 Jan 2022
Cited by 16 | Viewed by 4950
Abstract
The challenge of developing gene therapies for genetic forms of blindness is heightened by the heterogeneity of these conditions. However, mechanistic commonalities indicate key pathways that may be targeted in a gene-independent approach. Mitochondrial dysfunction and axon degeneration are common features of many [...] Read more.
The challenge of developing gene therapies for genetic forms of blindness is heightened by the heterogeneity of these conditions. However, mechanistic commonalities indicate key pathways that may be targeted in a gene-independent approach. Mitochondrial dysfunction and axon degeneration are common features of many neurodegenerative conditions including retinal degenerations. Here we explore the neuroprotective effect afforded by the absence of sterile alpha and Toll/interleukin-1 receptor motif-containing 1 (SARM1), a prodegenerative NADase, in a rotenone-induced mouse model of retinal ganglion cell loss and visual dysfunction. Sarm1 knockout mice retain visual function after rotenone insult, displaying preservation of photopic negative response following rotenone treatment in addition to significantly higher optokinetic response measurements than wild type mice following rotenone. Protection of spatial vision is sustained over time in both sexes and is accompanied by increased RGC survival and additionally preservation of axonal density in optic nerves of Sarm1−/− mice insulted with rotenone. Primary fibroblasts extracted from Sarm1−/− mice demonstrate an increased oxygen consumption rate relative to those from wild type mice, with significantly higher basal, maximal and spare respiratory capacity. Collectively, our data indicate that Sarm1 ablation increases mitochondrial bioenergetics and confers histological and functional protection in vivo in the mouse retina against mitochondrial dysfunction, a hallmark of many neurodegenerative conditions including a variety of ocular disorders. Full article
(This article belongs to the Special Issue Understanding the Molecular Mechanisms of Retinal Ganglion Cell Death after Optic Nerve Damage)
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15 pages, 3200 KiB  
Article
NGF Eye Administration Recovers the TrkB and Glutamate/GABA Marker Deficit in the Adult Visual Cortex Following Optic Nerve Crush
by Pamela Rosso, Elena Fico, Louise A. Mesentier-Louro, Viviana Triaca, Alessandro Lambiase, Paolo Rama and Paola Tirassa
Int. J. Mol. Sci. 2021, 22(18), 10014; https://doi.org/10.3390/ijms221810014 - 16 Sep 2021
Cited by 8 | Viewed by 2859
Abstract
Eye-drop recombinant human nerve growth factor (ed-rhNGF) has proved to recover the retina and optic nerve damage in animal models, including the unilateral optic nerve crush (ONC), and to improve visual acuity in humans. These data, associated with evidence that ed-rhNGF stimulates the [...] Read more.
Eye-drop recombinant human nerve growth factor (ed-rhNGF) has proved to recover the retina and optic nerve damage in animal models, including the unilateral optic nerve crush (ONC), and to improve visual acuity in humans. These data, associated with evidence that ed-rhNGF stimulates the brain derived neurotrophic factor (BDNF) in retina and cortex, suggests that NGF might exert retino-fugal effects by affecting BDNF and its receptor TrkB. To address these questions, their expression and relationship with the GABAergic and glutamatergic transmission markers, GAD65 and GAD67, vesicular inhibitory amino acid transporter (VGAT), and vesicular glutamate transporters 1 and 2 (VGLUT-1 and VGLUT-2) were investigated in adult ONC rats contralateral and ipsilateral visual cortex (VCx). Ed-rhNGF recovers the ONC-induced alteration of GABAergic and glutamatergic markers in contralateral VCx, induces an upregulation of TrkB, which is positively correlated with BDNF precursor (proBDNF) decrease in both VCx sides, and strongly enhances TrkB+ cell soma and neuronal endings surrounded by GAD65 immuno-reactive afferents. These findings contribute to enlarging the knowledge on the mechanism of actions and cellular targets of exogenously administrated NGF, and suggest that ed-rhNGF might act by potentiating the activity-dependent TrkB expression in GAD+ cells in VCx following retina damage and/or ONC. Full article
(This article belongs to the Special Issue Understanding the Molecular Mechanisms of Retinal Ganglion Cell Death after Optic Nerve Damage)
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Review

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24 pages, 1021 KiB  
Review
The Role of Axonal Transport in Glaucoma
by Mariana Santana Dias, Xiaoyue Luo, Vinicius Toledo Ribas, Hilda Petrs-Silva and Jan Christoph Koch
Int. J. Mol. Sci. 2022, 23(7), 3935; https://doi.org/10.3390/ijms23073935 - 1 Apr 2022
Cited by 21 | Viewed by 6091
Abstract
Glaucoma is a neurodegenerative disease that affects the retinal ganglion cells (RGCs) and leads to progressive vision loss. The first pathological signs can be seen at the optic nerve head (ONH), the structure where RGC axons leave the retina to compose the optic [...] Read more.
Glaucoma is a neurodegenerative disease that affects the retinal ganglion cells (RGCs) and leads to progressive vision loss. The first pathological signs can be seen at the optic nerve head (ONH), the structure where RGC axons leave the retina to compose the optic nerve. Besides damage of the axonal cytoskeleton, axonal transport deficits at the ONH have been described as an important feature of glaucoma. Axonal transport is essential for proper neuronal function, including transport of organelles, synaptic components, vesicles, and neurotrophic factors. Impairment of axonal transport has been related to several neurodegenerative conditions. Studies on axonal transport in glaucoma include analysis in different animal models and in humans, and indicate that its failure happens mainly in the ONH and early in disease progression, preceding axonal and somal degeneration. Thus, a better understanding of the role of axonal transport in glaucoma is not only pivotal to decipher disease mechanisms but could also enable early therapies that might prevent irreversible neuronal damage at an early time point. In this review we present the current evidence of axonal transport impairment in glaucomatous neurodegeneration and summarize the methods employed to evaluate transport in this disease. Full article
(This article belongs to the Special Issue Understanding the Molecular Mechanisms of Retinal Ganglion Cell Death after Optic Nerve Damage)
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