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Retinal Diseases and Cell Signaling
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Retinal Diseases and Cell Signaling

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 (30 December 2023) | Viewed by 11137

Special Issue Editor

Prof. Dr. Hiroshi Tomita

E-Mail Website
Guest Editor
Laboratory of Visual Neuroscience, Graduate Course in Biological Sciences, Division of Science and Engineering, Iwate University, 4-3-5 Ueda, Morioka 020-8551, Iwate, Japan
Interests: photoreceptor degeneration; retinal development; retinal gene therapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The numbers of patients with visual impaiment and blindness continue to rise year after year. As the top ranking diseases to lead to blindness, glaucoma, age-related macular degeneration (AMD), and retinitis pigmentosa (RP) are identified. There are variety of neurons in the retina and the visual impaiment occurrs even one type of neuron is degenerated. Numerous researches that investigated the mechanisms of retinal degeneration induced by diseases have contributed to develop the new types of therapies such as gene therapies and cell transplantation therapies. Therefore, the understanding of the diverse signalling molecules and signal transduction pathways of retinal degenerations is fundamental for develo** therapies. The scope of the special issue is to summarize and enlarge the knowledge of mechanisms in retinal degeneration and protection.

Therefore, authors are invited to submit original research and review articles which address the progress and current standing of basic researches in the retinal degeneration.

Topics include, but are not limited to:

  • New aspects of the mechanisms in retinal degenerative diseases
  • Techniques for the analysis and identification of retinal diseases
  • Evaluations of new treatments in animal studies

Prof. Dr. Hiroshi Tomita
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at mdpi.longhoe.net 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

  • retinal degeneration
  • regenerative medicine
  • gene therapy
  • electroretinogram
  • visually evoked potential
  • RNA-seq
  • apoptosis
  • animal model

Related Special Issues

Published Papers (7 papers)

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Research

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15 pages, 8091 KiB  
Article
The Role of microRNAs Related to Apoptosis for N-Methyl-d-Aspartic Acid-Induced Neuronal Cell Death in the Murine Retina
by Kohei Sone, Asami Mori, Kenji Sakamoto and Tsutomu Nakahara
Int. J. Mol. Sci. 2024, 25(2), 1106; https://doi.org/10.3390/ijms25021106 - 16 Jan 2024
Viewed by 964
Abstract
Glaucoma is one of the leading causes of acquired blindness and characterized by retinal ganglion cell (RGC) death. MicroRNAs are small noncoding RNAs that degrade their target mRNAs. Apoptosis is one of the common mechanisms leading to neuronal death in many neurodegenerative diseases, [...] Read more.
Glaucoma is one of the leading causes of acquired blindness and characterized by retinal ganglion cell (RGC) death. MicroRNAs are small noncoding RNAs that degrade their target mRNAs. Apoptosis is one of the common mechanisms leading to neuronal death in many neurodegenerative diseases, including glaucoma. In the present study, we identified microRNAs that modulate RGC death caused by the intravitreal injection of N-methyl-d-aspartic acid (NMDA). We found an upregulation of miR-29b and downregulation of miR-124 in the retina of the NMDA-injected eyes. The intravitreal injection of an miR-29b inhibitor 18 h before NMDA injection reduced RGC death and the downregulation of myeloid cell leukemia 1 (MCL-1), an anti-apoptotic factor, induced by intravitreal NMDA. The intravitreal injection of an miR-124 mimic 18 h before NMDA injection also reduced RGC death and the upregulation of B-cell/chronic lymphocytic leukemia lymphoma 2 (bcl-2)-associated X protein (Bax) and bcl-2 interacting protein (Bim), pro-apoptotic factors, induced by intravitreal NMDA. These data suggest that expressional changes in microRNA are involved in the excitotoxicity of RGCs, and that complement and/or inhibition of microRNA may be a potential therapeutic approach for the diseases related to the excitotoxicity of RGCs, such as glaucoma and retinal central artery occlusion. Full article
(This article belongs to the Special Issue Retinal Diseases and Cell Signaling)
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21 pages, 15718 KiB  
Article
The Phosphoproteome of the Rd1 Mouse Retina, a Model of Inherited Photoreceptor Degeneration, Changes after Protein Kinase G Inhibition
by Jiaming Zhou, Charlotte Welinder and Per Ekström
Int. J. Mol. Sci. 2023, 24(12), 9836; https://doi.org/10.3390/ijms24129836 - 7 Jun 2023
Cited by 1 | Viewed by 1319
Abstract
Retinitis pigmentosa (RP) is a frequent cause of blindness among the working population in industrial countries due to the inheritable death of photoreceptors. Though gene therapy was recently approved for mutations in the RPE65 gene, there is in general no effective treatment presently. [...] Read more.
Retinitis pigmentosa (RP) is a frequent cause of blindness among the working population in industrial countries due to the inheritable death of photoreceptors. Though gene therapy was recently approved for mutations in the RPE65 gene, there is in general no effective treatment presently. Previously, abnormally high levels of cGMP and overactivation of its dependent protein kinase (PKG) have been suggested as causative for the fatal effects on photoreceptors, making it meaningful to explore the cGMP-PKG downstream signaling for more pathological insights and novel therapeutic target development purposes. Here, we manipulated the cGMP-PKG system in degenerating retinas from the rd1 mouse model pharmacologically via adding a PKG inhibitory cGMP-analogue to organotypic retinal explant cultures. A combination of phosphorylated peptide enrichment and mass spectrometry was then applied to study the cGMP-PKG-dependent phosphoproteome. We identified a host of novel potential cGMP-PKG downstream substrates and related kinases using this approach and selected the RAF1 protein, which may act as both a substrate and a kinase, for further validation. This showed that the RAS/RAF1/MAPK/ERK pathway may be involved in retinal degeneration in a yet unclarified mechanism, thus deserving further investigation in the future. Full article
(This article belongs to the Special Issue Retinal Diseases and Cell Signaling)
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12 pages, 2982 KiB  
Article
Properties of a Single Amino Acid Residue in the Third Transmembrane Domain Determine the Kinetics of Ambient Light-Sensitive Channelrhodopsin
by Akito Hatakeyama, Eriko Sugano, Tatsuki Sayama, Yoshito Watanabe, Tomoya Suzuki, Kitako Tabata, Yuka Endo, Tetsuya Sakajiri, Tomokazu Fukuda, Taku Ozaki and Hiroshi Tomita
Int. J. Mol. Sci. 2023, 24(5), 5054; https://doi.org/10.3390/ijms24055054 - 6 Mar 2023
Cited by 1 | Viewed by 1502
Abstract
Channelrhodopsins have been utilized in gene therapy to restore vision in patients with retinitis pigmentosa and their channel kinetics are an important factor to consider in such applications. We investigated the channel kinetics of ComV1 variants with different amino acid residues at the [...] Read more.
Channelrhodopsins have been utilized in gene therapy to restore vision in patients with retinitis pigmentosa and their channel kinetics are an important factor to consider in such applications. We investigated the channel kinetics of ComV1 variants with different amino acid residues at the 172nd position. Patch clamp methods were used to record the photocurrents induced by stimuli from diodes in HEK293 cells transfected with plasmid vectors. The channel kinetics (τon and τoff) were considerably altered by the replacement of the 172nd amino acid and was dependent on the amino acid characteristics. The size of amino acids at this position correlated with τon and decay, whereas the solubility correlated with τon and τoff. Molecular dynamic simulation indicated that the ion tunnel constructed by H172, E121, and R306 widened due to H172A variant, whereas the interaction between A172 and the surrounding amino acids weakened compared with H172. The bottleneck radius of the ion gate constructed with the 172nd amino acid affected the photocurrent and channel kinetics. The 172nd amino acid in ComV1 is a key residue for determining channel kinetics as its properties alter the radius of the ion gate. Our findings can be used to improve the channel kinetics of channelrhodopsins. Full article
(This article belongs to the Special Issue Retinal Diseases and Cell Signaling)
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13 pages, 3073 KiB  
Article
Valdecoxib Protects against Cell Apoptosis Induced by Endoplasmic Reticulum Stress via the Inhibition of PERK-ATF4-CHOP Pathway in Experimental Glaucoma
by Zhaolin Gao, Min Li, Fei Yao, **aobo **a, Tianqi Duan, **gzhuo Meng, Yanxia Huang, Ye He, Adonira Saro and Jufang Huang
Int. J. Mol. Sci. 2022, 23(21), 12983; https://doi.org/10.3390/ijms232112983 - 26 Oct 2022
Cited by 7 | Viewed by 1816
Abstract
The purpose of this study was to investigate the effects of valdecoxib on the retina in retinal ischemia-reperfusion injury (IRI) and R28 cells following oxygen-glucose deprivation/recovery (OGD/R) injury, as well as the underlying mechanisms. Immunofluorescence and Cell Counting Kit-8 (CCK-8) analyses were used [...] Read more.
The purpose of this study was to investigate the effects of valdecoxib on the retina in retinal ischemia-reperfusion injury (IRI) and R28 cells following oxygen-glucose deprivation/recovery (OGD/R) injury, as well as the underlying mechanisms. Immunofluorescence and Cell Counting Kit-8 (CCK-8) analyses were used to identify the proper timepoint and concentration of valdecoxib’s protective effect on the R28 cells in the OGD/R model. Hematoxylin-eosin (HE) staining and immunofluorescence were used to explore valdecoxib’s effect on the retina and retina ganglion cell (RGC) in IRI. Cell apoptosis was determined by a TUNEL Apoptosis Detection Kit and Annexin V-FITC/PI flow cytometry. The expression levels of p-PERK, transcription factor 4 (ATF4), GRP78, CHOP, cleaved caspase 3, bax and bcl-2 were measured by Western blot analyses. The valdecoxib protected the R28 cells from OGD/R injury by decreasing the cell apoptosis rate, and it exerted a protective effect on retinas in I/R injury by inhibiting RGC apoptosis. The valdecoxib pretreatment reversed the expression of p-PERK, ATF4, CHOP, GRP78, cleaved caspase 3 and bax induced by the glaucomatous model. Meanwhile, the CCT020312 reversed the valdecoxib’s anti-apoptosis effect by activating PERK-ATF4-CHOP pathway-mediated endoplasmic reticulum (ER) stress. These findings suggest that valdecoxib protects against glaucomatous injury by inhibiting ER stress-induced apoptosis via the inhibition of the PERK-ATF4-CHOP pathway. Full article
(This article belongs to the Special Issue Retinal Diseases and Cell Signaling)
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Review

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12 pages, 489 KiB  
Review
Small Extracellular Vesicles and Oxidative Pathophysiological Mechanisms in Retinal Degenerative Diseases
by Francisco J. Romero, Manuel Diaz-Llopis, M. Inmaculada Romero-Gomez, Maria Miranda, Rebeca Romero-Wenz, Javier Sancho-Pelluz, Belén Romero, Maria Muriach and Jorge M. Barcia
Int. J. Mol. Sci. 2024, 25(3), 1618; https://doi.org/10.3390/ijms25031618 - 28 Jan 2024
Viewed by 1104
Abstract
This review focuses on the role of small extracellular vesicles in the pathophysiological mechanisms of retinal degenerative diseases. Many of these mechanisms are related to or modulated by the oxidative burden of retinal cells. It has been recently demonstrated that cellular communication in [...] Read more.
This review focuses on the role of small extracellular vesicles in the pathophysiological mechanisms of retinal degenerative diseases. Many of these mechanisms are related to or modulated by the oxidative burden of retinal cells. It has been recently demonstrated that cellular communication in the retina involves extracellular vesicles and that their rate of release and cargo features might be affected by the cellular environment, and in some instances, they might also be mediated by autophagy. The fate of these vesicles is diverse: they could end up in circulation being used as markers, or target neighbor cells modulating gene and protein expression, or eventually, in angiogenesis. Neovascularization in the retina promotes vision loss in diseases such as diabetic retinopathy and age-related macular degeneration. The importance of micro RNAs, either as small extracellular vesicles’ cargo or free circulating, in the regulation of retinal angiogenesis is also discussed. Full article
(This article belongs to the Special Issue Retinal Diseases and Cell Signaling)
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20 pages, 1001 KiB  
Review
Manifestation of Pathology in Animal Models of Diabetic Retinopathy Is Delayed from the Onset of Diabetes
by Samuel Cubillos and Andrius Kazlauskas
Int. J. Mol. Sci. 2024, 25(3), 1610; https://doi.org/10.3390/ijms25031610 - 28 Jan 2024
Cited by 1 | Viewed by 1247
Abstract
Diabetic retinopathy (DR) is the most common complication that develops in patients with diabetes mellitus (DM) and is the leading cause of blindness worldwide. Fortunately, sight-threatening forms of DR develop only after several decades of DM. This well-documented resilience to DR suggests that [...] Read more.
Diabetic retinopathy (DR) is the most common complication that develops in patients with diabetes mellitus (DM) and is the leading cause of blindness worldwide. Fortunately, sight-threatening forms of DR develop only after several decades of DM. This well-documented resilience to DR suggests that the retina is capable of protecting itself from DM-related damage and also that accumulation of such damage occurs only after deterioration of this resilience. Despite the enormous translational significance of this phenomenon, very little is known regarding the nature of resilience to DR. Rodent models of DR have been used extensively to study the nature of the DM-induced damage, i.e., cardinal features of DR. Many of these same animal models can be used to investigate resilience because DR is delayed from the onset of DM by several weeks or months. The purpose of this review is to provide a comprehensive overview of the literature describing the use of rodent models of DR in type-1 and type-2 diabetic animals, which most clearly document the delay between the onset of DM and the appearance of DR. These readily available experimental settings can be used to advance our current understanding of resilience to DR and thereby identify biomarkers and targets for novel, prevention-based approaches to manage patients at risk for develo** DR. Full article
(This article belongs to the Special Issue Retinal Diseases and Cell Signaling)
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49 pages, 1601 KiB  
Review
The Healthy and Diseased Retina Seen through Neuron–Glia Interactions
by Matheus H. Tempone, Vladimir P. Borges-Martins, Felipe César, Dio Pablo Alexandrino-Mattos, Camila S. de Figueiredo, Ícaro Raony, Aline Araujo dos Santos, Aline Teixeira Duarte-Silva, Mariana Santana Dias, Hércules Rezende Freitas, Elisabeth G. de Araújo, Victor Tulio Ribeiro-Resende, Marcelo Cossenza, Hilda P. Silva, Roberto P. de Carvalho, Ana L. M. Ventura, Karin C. Calaza, Mariana S. Silveira, Regina C. C. Kubrusly and Ricardo A. de Melo Reis
Int. J. Mol. Sci. 2024, 25(2), 1120; https://doi.org/10.3390/ijms25021120 - 17 Jan 2024
Viewed by 1906
Abstract
The retina is the sensory tissue responsible for the first stages of visual processing, with a conserved anatomy and functional architecture among vertebrates. To date, retinal eye diseases, such as diabetic retinopathy, age-related macular degeneration, retinitis pigmentosa, glaucoma, and others, affect nearly 170 [...] Read more.
The retina is the sensory tissue responsible for the first stages of visual processing, with a conserved anatomy and functional architecture among vertebrates. To date, retinal eye diseases, such as diabetic retinopathy, age-related macular degeneration, retinitis pigmentosa, glaucoma, and others, affect nearly 170 million people worldwide, resulting in vision loss and blindness. To tackle retinal disorders, the develo** retina has been explored as a versatile model to study intercellular signaling, as it presents a broad neurochemical repertoire that has been approached in the last decades in terms of signaling and diseases. Retina, dissociated and arranged as typical cultures, as mixed or neuron- and glia-enriched, and/or organized as neurospheres and/or as organoids, are valuable to understand both neuronal and glial compartments, which have contributed to revealing roles and mechanisms between transmitter systems as well as antioxidants, trophic factors, and extracellular matrix proteins. Overall, contributions in understanding neurogenesis, tissue development, differentiation, connectivity, plasticity, and cell death are widely described. A complete access to the genome of several vertebrates, as well as the recent transcriptome at the single cell level at different stages of development, also anticipates future advances in providing cues to target blinding diseases or retinal dysfunctions. Full article
(This article belongs to the Special Issue Retinal Diseases and Cell Signaling)
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