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Retinal Degeneration and Protection
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Retinal Degeneration and Protection

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 (24 June 2022) | Viewed by 11443

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 developing 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. Hiroshi Tomita
Guest Editor

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.

Related Special Issue

Published Papers (5 papers)

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Research

14 pages, 2853 KiB  
Article
SIG-1451, a Novel, Non-Steroidal Anti-Inflammatory Compound, Attenuates Light-Induced Photoreceptor Degeneration by Affecting the Inflammatory Process
by Yuki Kikuchi, Eriko Sugano, Shiori Yuki, Kitako Tabata, Yuka Endo, Yuya Takita, Reina Onoguchi, Taku Ozaki, Tomokazu Fukuda, Yoshihiro Takai, Takahiro Kurose, Koichi Tanaka, Yoichi Honma, Eduardo Perez, Maxwell Stock, José R. Fernández, Masanori Tamura, Michael Voronkov, Jeffry B. Stock and Hiroshi Tomita
Int. J. Mol. Sci. 2022, 23(15), 8802; https://doi.org/10.3390/ijms23158802 - 8 Aug 2022
Cited by 2 | Viewed by 1978
Abstract
Age-related macular degeneration is a progressive retinal disease that is associated with factors such as oxidative stress and inflammation. In this study, we evaluated the protective effects of SIG-1451, a non-steroidal anti-inflammatory compound developed for treating atopic dermatitis and known to inhibit Toll-like [...] Read more.
Age-related macular degeneration is a progressive retinal disease that is associated with factors such as oxidative stress and inflammation. In this study, we evaluated the protective effects of SIG-1451, a non-steroidal anti-inflammatory compound developed for treating atopic dermatitis and known to inhibit Toll-like receptor 4, in light-induced photoreceptor degeneration. SIG-1451 was intraperitoneally injected into rats once per day before exposure to 1000 lx light for 24 h; one day later, optical coherence tomography showed a decrease in retinal thickness, and electroretinogram (ERG) amplitude was also found to have decreased 3 d after light exposure. Moreover, SIG-1451 partially protected against this decrease in retinal thickness and increase in ERG amplitude. One day after light exposure, upregulation of inflammatory response-related genes was observed, and SIG-1451 was found to inhibit this upregulation. Iba-1, a microglial marker, was suppressed in SIG-1451-injected rats. To investigate the molecular mechanism underlying these effects, we used lipopolysaccharide (LPS)-stimulated rat immortalised Müller cells. The upregulation of C-C motif chemokine 2 by LPS stimulation was significantly inhibited by SIG-1451 treatment, and Western blot analysis revealed a decrease in phosphorylated I-κB levels. These results indicate that SIG-1451 indirectly protects photoreceptor cells by attenuating light damage progression, by affecting the inflammatory responses. Full article
(This article belongs to the Special Issue Retinal Degeneration and Protection)
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19 pages, 5653 KiB  
Article
Deficiency in Retinal TGFβ Signaling Aggravates Neurodegeneration by Modulating Pro-Apoptotic and MAP Kinase Pathways
by Christina B. Bielmeier, Sabrina I. Schmitt, Nikolai Kleefeldt, Stefaniya K. Boneva, Anja Schlecht, Mario Vallon, Ernst R. Tamm, Jost Hillenkamp, Süleyman Ergün, Andreas Neueder and Barbara M. Braunger
Int. J. Mol. Sci. 2022, 23(5), 2626; https://doi.org/10.3390/ijms23052626 - 27 Feb 2022
Cited by 8 | Viewed by 2052
Abstract
Transforming growth factor β (TGFβ) signaling has manifold functions such as regulation of cell growth, differentiation, migration, and apoptosis. Moreover, there is increasing evidence that it also acts in a neuroprotective manner. We recently showed that TGFβ receptor type 2 (Tgfbr2) [...] Read more.
Transforming growth factor β (TGFβ) signaling has manifold functions such as regulation of cell growth, differentiation, migration, and apoptosis. Moreover, there is increasing evidence that it also acts in a neuroprotective manner. We recently showed that TGFβ receptor type 2 (Tgfbr2) is upregulated in retinal neurons and Müller cells during retinal degeneration. In this study we investigated if this upregulation of TGFβ signaling would have functional consequences in protecting retinal neurons. To this end, we analyzed the impact of TGFβ signaling on photoreceptor viability using mice with cell type-specific deletion of Tgfbr2 in retinal neurons and Müller cells (Tgfbr2ΔOC) in combination with a genetic model of photoreceptor degeneration (VPP). We examined retinal morphology and the degree of photoreceptor degeneration, as well as alterations of the retinal transcriptome. In summary, retinal morphology was not altered due to TGFβ signaling deficiency. In contrast, VPP-induced photoreceptor degeneration was drastically exacerbated in double mutant mice (Tgfbr2ΔOC; VPP) by induction of pro-apoptotic genes and dysregulation of the MAP kinase pathway. Therefore, TGFβ signaling in retinal neurons and Müller cells exhibits a neuroprotective effect and might pose promising therapeutic options to attenuate photoreceptor degeneration in humans. Full article
(This article belongs to the Special Issue Retinal Degeneration and Protection)
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12 pages, 16760 KiB  
Article
Hypoxia Inhibits Subretinal Inflammation Resolution Thrombospondin-1 Dependently
by Sara Touhami, Fanny Béguier, Tianxiang Yang, Sébastien Augustin, Christophe Roubeix, Frederic Blond, Jean Baptiste Conart, José Alain Sahel, Bahram Bodaghi, Cécile Delarasse, Xavier Guillonneau and Florian Sennlaub
Int. J. Mol. Sci. 2022, 23(2), 681; https://doi.org/10.3390/ijms23020681 - 8 Jan 2022
Cited by 7 | Viewed by 1939
Abstract
Hypoxia is potentially one of the essential triggers in the pathogenesis of wet age-related macular degeneration (wetAMD), characterized by choroidal neovascularization (CNV) which is driven by the accumulation of subretinal mononuclear phagocytes (MP) that include monocyte-derived cells. Here we show that systemic hypoxia [...] Read more.
Hypoxia is potentially one of the essential triggers in the pathogenesis of wet age-related macular degeneration (wetAMD), characterized by choroidal neovascularization (CNV) which is driven by the accumulation of subretinal mononuclear phagocytes (MP) that include monocyte-derived cells. Here we show that systemic hypoxia (10% O2) increased subretinal MP infiltration and inhibited inflammation resolution after laser-induced subretinal injury in vivo. Accordingly, hypoxic (2% O2) human monocytes (Mo) resisted elimination by RPE cells in co-culture. In Mos from hypoxic mice, Thrombospondin 1 mRNA (Thbs1) was most downregulated compared to normoxic animals and hypoxia repressed Thbs-1 expression in human monocytes in vitro. Hypoxic ambient air inhibited MP clearance during the resolution phase of laser-injury in wildtype animals, but had no effect on the exaggerated subretinal MP infiltration observed in normoxic Thbs1−/−-mice. Recombinant Thrombospondin 1 protein (TSP-1) completely reversed the pathogenic effect of hypoxia in Thbs1−/−-mice, and accelerated inflammation resolution and inhibited CNV in wildtype mice. Together, our results demonstrate that systemic hypoxia disturbs TSP-1-dependent subretinal immune suppression and promotes pathogenic subretinal inflammation and can be therapeutically countered by local recombinant TSP-1. Full article
(This article belongs to the Special Issue Retinal Degeneration and Protection)
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13 pages, 12183 KiB  
Article
Structural and Functional Change in Albino Rat Retina Induced by Various Visible Light Wavelengths
by Sachiko Kaidzu, Tsutomu Okuno, Masaki Tanito and Akihiro Ohira
Int. J. Mol. Sci. 2022, 23(1), 309; https://doi.org/10.3390/ijms23010309 - 28 Dec 2021
Cited by 3 | Viewed by 1593
Abstract
The effects of visible light, from short to long wavelengths, on the retina were investigated functionally and histologically. The left eyes of Sprague–Dawley albino rats (6-weeks old, n = 6 for each wavelength) were exposed to seven narrow-band wavelengths (central wavelengths, 421, 441, [...] Read more.
The effects of visible light, from short to long wavelengths, on the retina were investigated functionally and histologically. The left eyes of Sprague–Dawley albino rats (6-weeks old, n = 6 for each wavelength) were exposed to seven narrow-band wavelengths (central wavelengths, 421, 441, 459, 501, 541, 581, and 615 nm) with bandwidths of 16 to 29 nm (half bandwidth, ±8–14.5 nm) using a xenon lamp source with bandpass filters at the retinal radiant exposures of 340 and 680 J/cm2. The right unexposed eyes served as controls. Seven days after exposure, flash electroretinograms (ERGs) were recorded, and the outer nuclear layer (ONL) thickness was measured. Compared to the unexposed eyes, significant reductions in the a- and b-wave ERG amplitudes were seen in eyes exposed to 460-nm or shorter wavelengths of light. The ONL thickness near the optic nerve head also tended to decrease with exposure to shorter wavelengths. The decreased ERG amplitudes and ONL thicknesses were most prominent in eyes exposed to 420-nm light at both radiant exposures. When the wavelengths were the same, the higher the amount of radiant exposure and the stronger the damage. Compared to the unexposed eyes, the a- and b-waves did not decrease significantly in eyes exposed to 500-nm or longer wavelength light. The results indicate that the retinal damage induced by visible light observed in albino rats depends on the wavelength and energy level of the exposed light. Full article
(This article belongs to the Special Issue Retinal Degeneration and Protection)
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12 pages, 7058 KiB  
Article
LRG1 Expression Is Elevated in the Eyes of Patients with Neovascular Age-Related Macular Degeneration
by Lucia Mundo, Gian Marco Tosi, Stefano Lazzi, Grazia Pertile, Barbara Parolini, Giovanni Neri, Matteo Posarelli, Elena De Benedetto, Tommaso Bacci, Ennio Silvestri, Maria Chiara Siciliano, Stefano Barbera, Maurizio Orlandini, John Greenwood, Stephen E. Moss and Federico Galvagni
Int. J. Mol. Sci. 2021, 22(16), 8879; https://doi.org/10.3390/ijms22168879 - 18 Aug 2021
Cited by 11 | Viewed by 2945
Abstract
Leucine-rich a-2-glycoprotein 1 (LRG1) is a candidate therapeutic target for treating the neovascular form of age-related macular degeneration (nvAMD). In this study we examined the expression of LRG1 in eyes of nvAMD patients. Choroidal neovascular membranes (CNVMs) from patients who underwent submacular surgery [...] Read more.
Leucine-rich a-2-glycoprotein 1 (LRG1) is a candidate therapeutic target for treating the neovascular form of age-related macular degeneration (nvAMD). In this study we examined the expression of LRG1 in eyes of nvAMD patients. Choroidal neovascular membranes (CNVMs) from patients who underwent submacular surgery for retinal pigment epithelium–choroid graft transplantation were collected from 5 nvAMD patients without any prior intravitreal anti-VEGF injection, and from six patients who received intravitreal anti-VEGF injections before surgery. As controls free of nvAMD, retina sections were obtained from the eyes resected from a patient with lacrimal sac tumor and from a patient with neuroblastoma. CNVMs were immunostained for CD34, LRG1, and α-smooth muscle actin (α-SMA). Aqueous humor samples were collected from 58 untreated-naïve nvAMD patients prior to the intravitreal injection of anti-VEGF and 51 age-matched cataract control patients, and LRG1 concentration was measured by ELISA. The level of LRG1 immunostaining is frequently high in both the endothelial cells of the blood vessels, and myofibroblasts in the surrounding tissue of CNVMs of treatment-naïve nvAMD patients. Furthermore, the average concentration of LRG1 was significantly higher in the aqueous humor of nvAMD patients than in controls. These observations provide a strong experimental basis and scientific rationale for the progression of a therapeutic anti-LRG1 monoclonal antibody into clinical trials with patients with nvAMD. Full article
(This article belongs to the Special Issue Retinal Degeneration and Protection)
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