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Cells
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Injury, Neurodegeneration, and Regeneration of Retinal Ganglion Cells
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Injury, Neurodegeneration, and Regeneration of Retinal Ganglion Cells

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Nervous System".

Deadline for manuscript submissions: 30 November 2024 | Viewed by 5602

Special Issue Editors

Prof. Dr. Ning Tian

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Guest Editor
Department of Ophthalmology and Visual Sciences, University of Utah School of Medicine, Salt Lake City, UT, USA
Interests: RGC death and protection; retinal circuitry development; activity-dependent synaptic plasticity; retinal ganglion cells
Dr. Lin Gan

E-Mail Website
Guest Editor
Department of Neuroscience & Regenerative Medicine, Medical College of Georgia at Augusta University, Augusta, GA 30912, USA
Interests: retinal development with a focus on the roles of transcription factors in determining retinal neuron identities
Dr. Xian-Jie Yang

E-Mail Website
Guest Editor
Stein Eye Institute, University of California, David Geffen School of Medicine, Los Angeles, CA 90095, USA
Interests: retinal development; stem cell-based human retinal organoids; neuroprotection mechanisms; viral mediated gene delivery and therapy
Dr. Yongling Zhu

E-Mail Website
Guest Editor
Department of Ophthalmology and Physiology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA
Interests: retinal circuits; RGCs; amacrine cells; mouse genetics; viral vector technologies; electrophysiology; functional imaging

Special Issue Information

Dear Colleagues,

Retinal ganglion cells (RGCs) are the output neurons of the retina. RGC death is crucial in many retinal diseases leading to blindness, such as glaucoma, optic neuritis, diabetic retinopathy, pathological myopia, and optic nerve injury. Since the loss of RGCs results in the irreversible loss of vision and no effective treatment is available to date, effectively preventing RGC death or regenerating RGCs under disease conditions must be addressed in the research. However, the death of RGCs in these disease conditions involves multiple molecular and cellular mechanisms. In addition, numerous studies have demonstrated that RGCs present significant subtype-specific vulnerabilities to pathological insults. Therefore, the research requires rigorous efforts and a thorough understanding of distinct but interlinked processes, including the molecular mechanisms that regulate RGC differentiation and survival, genes that promote RGC regeneration, proteins or small molecules that prevent RGC death, and the mechanisms that control the integration of regenerated or transplanted RGCs into existing neuronal circuits. The research also requires the development of innovative techniques to activate intrinsic stem cells for RGC regeneration or to promote the ex vivo growth of RGCs for transplantation.

The aim of this Special Issue of Cells is to collate the latest high-quality articles written by researchers working in all areas related to the injury, degeneration, survival, and regeneration of vertebrate RGCs in a collection of original research articles, reviews, and communications. The scope will be comprehensive, including the genetic, molecular, anatomical, physiological, and pathophysiological mechanisms and signaling pathways that control RGC development, degeneration, and regeneration under normal and disease conditions.

Prof. Dr. Ning Tian
Dr. Lin Gan
Dr. Xian-Jie Yang
Dr. Yongling Zhu
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • retinal ganglion cells
  • RGC development
  • RGC degeneration
  • RGC and axonal regeneration
  • molecular mechanism
  • RGC survival
  • retina
  • signal transduction pathways
  • RGC injury
  • glaucoma
  • RGC transplantation
  • retinal organoid
  • optic neuropathy
  • retinal circuits

Published Papers (3 papers)

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Research

23 pages, 6316 KiB  
Article
The Inflammasome-Dependent Dysfunction and Death of Retinal Ganglion Cells after Repetitive Intraocular Pressure Spikes
by Markus Spurlock, Weijun An, Galina Reshetnikova, Rong Wen, Hua Wang, Michelle Braha, Gabriela Solis, Stefan Kurtenbach, Orlando J. Galindez, Juan Pablo de Rivero Vaccari, Tsung-Han Chou, Vittorio Porciatti and Valery I. Shestopalov
Cells 2023, 12(22), 2626; https://doi.org/10.3390/cells12222626 - 15 Nov 2023
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Abstract
The dysfunction and selective loss of retinal ganglion cells (RGCs) is a known cause of vision loss in glaucoma and other neuropathies, where ocular hypertension (OHT) is the major risk factor. We investigated the impact of transient non-ischemic OHT spikes (spOHT) on RGC [...] Read more.
The dysfunction and selective loss of retinal ganglion cells (RGCs) is a known cause of vision loss in glaucoma and other neuropathies, where ocular hypertension (OHT) is the major risk factor. We investigated the impact of transient non-ischemic OHT spikes (spOHT) on RGC function and viability in vivo to identify cellular pathways linking low-grade repetitive mechanical stress to RGC pathology. We found that repetitive spOHT had an unexpectedly high impact on intraocular homeostasis and RGC viability, while exposure to steady OHT (stOHT) of a similar intensity and duration failed to induce pathology. The repetitive spOHT induced the rapid activation of the inflammasome, marked by the upregulation of NLRP1, NLRP3, AIM2, caspases -1, -3/7, -8, and Gasdermin D (GSDMD), and the release of interleukin-1β (IL-1β) and other cytokines into the vitreous. Similar effects were also detected after 5 weeks of exposure to chronic OHT in an induced glaucoma model. The onset of these immune responses in both spOHT and glaucoma models preceded a 50% deficit in pattern electroretinogram (PERG) amplitude and a significant loss of RGCs 7 days post-injury. The inactivation of inflammasome complexes in Nlrp1−/−, Casp1−/−, and GsdmD−/− knockout animals significantly suppressed the spOHT-induced inflammatory response and protected RGCs. Our results demonstrate that mechanical stress produced by acute repetitive spOHT or chronic OHT is mechanistically linked to inflammasome activation, which leads to RGC dysfunction and death. Full article
(This article belongs to the Special Issue Injury, Neurodegeneration, and Regeneration of Retinal Ganglion Cells)
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20 pages, 12210 KiB  
Article
Inducible Rbpms-CreERT2 Mouse Line for Studying Gene Function in Retinal Ganglion Cell Physiology and Disease
by Luming Guo, Xiaoling Xie, Jing Wang, Haiyan Xiao, Shuchun Li, Mei Xu, Ebenezer Quainoo, Rithwik Koppaka, Jiaping Zhuo, Sylvia B. Smith and Lin Gan
Cells 2023, 12(15), 1951; https://doi.org/10.3390/cells12151951 - 27 Jul 2023
Viewed by 1972
Abstract
Retinal ganglion cells (RGCs) are the sole output neurons conveying visual stimuli from the retina to the brain, and dysfunction or loss of RGCs is the primary determinant of visual loss in traumatic and degenerative ocular conditions. Currently, there is a lack of [...] Read more.
Retinal ganglion cells (RGCs) are the sole output neurons conveying visual stimuli from the retina to the brain, and dysfunction or loss of RGCs is the primary determinant of visual loss in traumatic and degenerative ocular conditions. Currently, there is a lack of RGC-specific Cre mouse lines that serve as invaluable tools for manipulating genes in RGCs and studying the genetic basis of RGC diseases. The RNA-binding protein with multiple splicing (RBPMS) is identified as the specific marker of all RGCs. Here, we report the generation and characterization of a knock-in mouse line in which a P2A-CreERT2 coding sequence is fused in-frame to the C-terminus of endogenous RBPMS, allowing for the co-expression of RBPMS and CreERT2. The inducible Rbpms-CreERT2 mice exhibited a high recombination efficiency in activating the expression of the tdTomato reporter gene in nearly all adult RGCs as well as in differentiated RGCs starting at E13.5. Additionally, both heterozygous and homozygous Rbpms-CreERT2 knock-in mice showed no detectable defect in the retinal structure, visual function, and transcriptome. Together, these results demonstrated that the Rbpms-CreERT2 knock-in mouse can serve as a powerful and highly desired genetic tool for lineage tracing, genetic manipulation, retinal physiology study, and ocular disease modeling in RGCs. Full article
(This article belongs to the Special Issue Injury, Neurodegeneration, and Regeneration of Retinal Ganglion Cells)
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15 pages, 5031 KiB  
Article
Neuronal p58IPK Protects Retinal Ganglion Cells Independently of Macrophage/Microglia Activation in Ocular Hypertension
by Todd McLaughlin, Jinli Wang, Liyun Jia, Fuguo Wu, Yaqin Wang, Joshua J. Wang, Xiuqian Mu and Sarah X. Zhang
Cells 2023, 12(12), 1558; https://doi.org/10.3390/cells12121558 - 06 Jun 2023
Cited by 1 | Viewed by 1609
Abstract
p58IPK is a multifaceted endoplasmic reticulum (ER) chaperone and a regulator of eIF2α kinases involved in a wide range of cellular processes including protein synthesis, ER stress response, and macrophage-mediated inflammation. Systemic deletion of p58IPK leads to age-related loss of retinal [...] Read more.
p58IPK is a multifaceted endoplasmic reticulum (ER) chaperone and a regulator of eIF2α kinases involved in a wide range of cellular processes including protein synthesis, ER stress response, and macrophage-mediated inflammation. Systemic deletion of p58IPK leads to age-related loss of retinal ganglion cells (RGC) and exacerbates RGC damage induced by ischemia/reperfusion and increased intraocular pressure (IOP), suggesting a protective role of p58IPK in the retina. However, the mechanisms remain elusive. Herein, we investigated the cellular mechanisms underlying the neuroprotection action of p58IPK using conditional knockout (cKO) mouse lines where p58IPK is deleted in retinal neurons (Chx10-p58IPK cKO) or in myeloid cells (Lyz2-p58IPK cKO). In addition, we overexpressed p58IPK by adeno-associated virus (AAV) in the retina to examine the effect of p58IPK on RGC survival after ocular hypertension (OHT) in wild type (WT) mice. Our results show that overexpression of p58IPK by AAV significantly improved RGC survival after OHT in WT mice, suggesting a protective effect of p58IPK on reducing RGC injury. Conditional knockout of p58IPK in retinal neurons or in myeloid cells did not alter retinal structure or cellular composition. However, a significant reduction in the b wave of light-adapted electroretinogram (ERG) was observed in Chx10-p58IPK cKO mice. Deletion of p58IPK in retinal neurons exacerbates RGC loss at 14 days after OHT. In contrast, deficiency of p58IPK in myeloid cells increased the microglia/macrophage activation but had no effect on RGC loss. We conclude that deletion of p58IPK in macrophages increases their activation, but does not influence RGC survival. These results suggest that the neuroprotective action of p58IPK is mediated by its expression in retinal neurons, but not in macrophages. Therefore, targeting p58IPK specifically in retinal neurons is a promising approach for the treatment of neurodegenerative retinal diseases including glaucoma. Full article
(This article belongs to the Special Issue Injury, Neurodegeneration, and Regeneration of Retinal Ganglion Cells)
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