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Neurobiology of Vision in Health and Disease
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Neurobiology of Vision in Health and Disease

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

Deadline for manuscript submissions: closed (15 July 2023) | Viewed by 5187

Special Issue Editors

Dr. Ifat Sher-Rosenthal

E-Mail Website
Guest Editor
1. Goldschleger Eye Institute, Sheba Medical Center, Tel Hashomer, Israel
2. Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel
Interests: retina; retinitis pigmentosa; iPSC; animal models; retinal cultures; drug discovery
Prof. Dr. Ygal Rotenstreich

E-Mail Website
Guest Editor
1. Goldschleger Eye Institute, Sheba Medical Center, Tel Hashomer, Israel
2. Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel
3. Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, Israel
Interests: electrophysiology; retinal function; retinal degeneration; ocular imaging; drug discovery

Special Issue Information

Dear Colleagues, 

Vision is a concert function of retinal photoreceptors, bipolar and horizontal cells, retinal ganglion cells that form the optic nerve, and the downstream neurons in the visual cortex. Retinal pigment epithelium (RPE), Amacrine and Müller cells support and regulate neuroretinal signaling. Advances in genetic testing led to the identification of over 260 genes related to vision loss due to retinal degeneration, majority of them are expressed in photoreceptors and supporting RPE. Some of these genes are related directly to signal transduction and retinal cell survival whereas others are modifier genes that modify retinal degeneration progression. Several genes are associated with high risk to develop glaucoma and age-related macular degeneration. Understanding the mechanisms by which mutations in these genes lead to dysfunction and death of neuroretinal cells may shed light on the molecular pathways underlying neuroretinal cell function in homeostasis and is predicted to lead to drug discovery to prevent vision loss. Although the eye is considered immune-privileged, growing evidence indicates the involvement of the immune system in neurodegenerative processes in the neuro-retina. The balance between beneficial and harmful activation of retinal glial cells may ameliorate or accelerate neurodegeneration of retinal photoreceptors and ganglion cells.

This special issue will focus on genetics, epigenetics and signaling pathways in neuroretinal cells in homeostasis and in disease. We invite research studies and reviews on genetics of retinal, macular and optic nerve degeneration, gene expression patterns in neuroretinal cells and those associated with retinal cell dysfunction and death, retinal cell metabolism, studies exploring the crosstalk between inflammation, microglial cell activation and neuroretinal cell function, as well as studies on innovative therapeutic interventions and drug delivery.

Dr. Ifat Sher-Rosenthal
Prof. Dr. Ygal Rotenstreich
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • vision
  • retina
  • glaucoma
  • retinal development
  • photoreceptors
  • retinal degeneration
  • retinal ganglion cells
  • phototransduction
  • retinal microglia
  • oxydative stress
  • RPE
  • amacrine cells
  • Müller cells

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Published Papers (2 papers)

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Research

17 pages, 7213 KiB  
Article
Inhibition of the MAPK/c-Jun-EGR1 Pathway Decreases Photoreceptor Cell Death in the rd1 Mouse Model for Inherited Retinal Degeneration
by Yujie Dong, Wenrong Xu, Yan Li, Chunling Wei, Yunzhang Hu, Zhulin Hu, François Paquet-Durand and Kangwei Jiao
Int. J. Mol. Sci. 2022, 23(23), 14600; https://doi.org/10.3390/ijms232314600 - 23 Nov 2022
Cited by 8 | Viewed by 2570
Abstract
Retinitis pigmentosa (RP) is a group of inherited retinal dystrophies that typically results in photoreceptor cell death and vision loss. Here, we explored the effect of early growth response-1 (EGR1) expression on photoreceptor cell death in Pde6brd1 (rd1) mice and [...] Read more.
Retinitis pigmentosa (RP) is a group of inherited retinal dystrophies that typically results in photoreceptor cell death and vision loss. Here, we explored the effect of early growth response-1 (EGR1) expression on photoreceptor cell death in Pde6brd1 (rd1) mice and its mechanism of action. To this end, single-cell RNA-seq (scRNA-seq) was used to identify differentially expressed genes in rd1 and congenic wild-type (WT) mice. Chromatin immunoprecipitation (ChIP), the dual-luciferase reporter gene assay, and western blotting were used to verify the relationship between EGR1 and poly (ADP-ribose) polymerase-1 (PARP1). Immunofluorescence staining was used to assess PARP1 expression after silencing or overexpression of EGR1. Photoreceptor cell death was assessed using the TUNEL assay following silencing/overexpression of EGR1 or administration of MAPK/c-Jun pathway inhibitors tanzisertib and PD98059. Our results showed differential expression of ERG1 in rd1 and WT mice via scRNA-seq analysis. The ChIP assay demonstrated EGR1 binding to the PARP1 promoter region. The dual-luciferase reporter gene assay and western blotting results revealed that EGR1 upregulated PARP1 expression. Additionally, the TUNEL assay showed that silencing EGR1 effectively reduced photoreceptor cell death. Similarly, the addition of tanzisertib and PD98059 reduced the expression of c-Jun and EGR1 and decreased photoreceptor cell death. Our study revealed that inhibition of the MAPK/c-Jun pathway reduced the expression of EGR1 and PARP1 and prevented photoreceptor cell death. These results highlight the importance of EGR1 for photoreceptor cell death and identify a new avenue for therapeutic interventions in RP. Full article
(This article belongs to the Special Issue Neurobiology of Vision in Health and Disease)
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23 pages, 2044 KiB  
Article
Binding of Alpha-Crystallin to Cortical and Nuclear Lens Lipid Membranes Derived from a Single Lens
by Raju Timsina, Samantha Wellisch, Dieter Haemmerle and Laxman Mainali
Int. J. Mol. Sci. 2022, 23(19), 11295; https://doi.org/10.3390/ijms231911295 - 25 Sep 2022
Cited by 9 | Viewed by 1881
Abstract
Several studies reported that α-crystallin concentrations in the eye lens cytoplasm decrease with a corresponding increase in membrane-bound α-crystallin with age and cataracts. The influence of the lipid and cholesterol composition difference between cortical membrane (CM) and nuclear membrane (NM) on α-crystallin binding [...] Read more.
Several studies reported that α-crystallin concentrations in the eye lens cytoplasm decrease with a corresponding increase in membrane-bound α-crystallin with age and cataracts. The influence of the lipid and cholesterol composition difference between cortical membrane (CM) and nuclear membrane (NM) on α-crystallin binding to membranes is still unclear. This study uses the electron paramagnetic resonance (EPR) spin-labeling method to investigate the α-crystallin binding to bovine CM and NM derived from the total lipids extracted from a single lens. Compared to CMs, NMs have a higher percentage of membrane surface occupied by α-crystallin and binding affinity, correlating with less mobility and more order below and on the surface of NMs. α-Crystallin binding to CM and NM decreases mobility with no significant change in order and hydrophobicity below and on the surface of membranes. Our results suggest that α-crystallin mainly binds on the surface of bovine CM and NM and such surface binding of α-crystallin to membranes in clear and young lenses may play a beneficial role in membrane stability. However, with decreased cholesterol content within the CM, which mimics the decreased cholesterol content in the cataractous lens membrane, α-crystallin binding increases the hydrophobicity below the membrane surface, indicating that α-crystallin binding forms a hydrophobic barrier for the passage of polar molecules, supporting the barrier hypothesis in developing cataracts. Full article
(This article belongs to the Special Issue Neurobiology of Vision in Health and Disease)
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