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Molecular Mechanisms of Retinal Diseases: An Update

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (20 June 2024) | Viewed by 1255

Special Issue Editor


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Guest Editor
Department of Neuroscience, University of Montreal Hospital Research Centre (CRCHUM), Montreal, QC H3G 1A4, Canada
Interests: glaucoma; retinal ganglion cells; clinical ophthalmology; eye diseases; retinal imaging; visual neuroscience

Special Issue Information

Dear Colleagues, 

Homeostatic processes of retinal structure and function are orchestrated by neurons, glial cells, and vasculature; their disruption leads to remodeling and degeneration in the pathophysiology of vision-threatening retinal diseases.

Recent advances in molecular biology have enabled state-of-the-art imaging techniques by using multiphoton microscopy, genome editing by using the CRISPR/Cas9 system, novel disease modeling by using iPS cells, and multi-omics analyses, including single-cell RNA seq.

The above have allowed for the visualization of molecular dynamics in vivo, the establishment of disease-specific genetic modifications as well as models, and an understanding of complex intracellular diversity, resulting in the identification of promising molecules that cause critical pathologies and the determination of therapeutic strategies with which to restore damaged tissues and their functions.

This Special Issue aims to discuss and summarize insights into new molecular mechanisms and potential therapeutics for retinal degenerative diseases, such as age-related macular degeneration, diabetic retinopathy, inherited retinal diseases, glaucoma, myopia, and retinal vascular diseases.

In this Special Issue, we welcome original research or review articles on the pathogenesis of retinal diseases and their therapeutic targets via the use of novel molecular biological approaches.

Dr. Yukihiro Shiga
Guest Editor

Manuscript Submission Information

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Keywords

  • in vivo imaging
  • CRISPR/Cas9
  • iPS cells
  • single-cell RNA seq
  • age-related macular degeneration
  • diabetic retinopathy
  • inherited retinal diseases
  • glaucoma
  • myopia
  • retinal vascular diseases

Published Papers (1 paper)

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Research

13 pages, 3579 KiB  
Article
JP4-039, a Mitochondria-Targeted Nitroxide, Mitigates the Effect of Apoptosis and Inflammatory Cell Migration in the Irradiated Mouse Retina
by Jennifer O. Adeghate, Michael W. Epperly, Katherine Anne Davoli, Kira L. Lathrop, Peter Wipf, Wen Hou, Renee Fisher, Stephanie Thermozier, M. Saiful Huq, Jose-Alain Sahel, Joel S. Greenberger and Andrew W. Eller
Int. J. Mol. Sci. 2024, 25(12), 6515; https://doi.org/10.3390/ijms25126515 - 13 Jun 2024
Viewed by 907
Abstract
We hypothesize that the injection of JP4-039, a mitochondria-targeted nitroxide, prior to irradiation of the mouse retina may decrease apoptosis and reduce neutrophil and macrophage migration into the retina. In our study, we aimed to examine the effects of JP4-039 in the mouse [...] Read more.
We hypothesize that the injection of JP4-039, a mitochondria-targeted nitroxide, prior to irradiation of the mouse retina may decrease apoptosis and reduce neutrophil and macrophage migration into the retina. In our study, we aimed to examine the effects of JP4-039 in the mouse retina using fluorescent microscopy, a terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, and flow cytometry. Forty-five mice and one eye per mouse were used. In Group 1, fluorescent microscopy was used to determine retinal uptake of 10 µL (0.004 mg/µL) of intravitreally injected BODIPY-labeled JP4-039 at 0, 15, and 60 min after injection. In Group 2, the TUNEL assay was performed to investigate the rate of apoptosis after irradiation in addition to JP4-039 injection, compared to controls. In Group 3, flow cytometry was used to determine the extent of inflammatory cell migration into the retina after irradiation in addition to JP4-039 injection, compared to controls. Maximal retinal uptake of JP4-039 was 15 min after intravitreal injection (p < 0.0001). JP4-039-treated eyes had lower levels of retinal apoptosis (35.8 ± 2.5%) than irradiated controls (49.0 ± 2.7%; p = 0.0066) and demonstrated reduced migration of N1 cells (30.7 ± 11.7% vs. 77.7 ± 5.3% controls; p = 0.004) and M1 cells (76.6 ± 4.2 vs. 88.1 ± 3.7% controls, p = 0.04). Pretreatment with intravitreally injected JP4-039 reduced apoptosis and inflammatory cell migration in the irradiated mouse retina, marking the first confirmed effect of this molecule in retinal tissue. Further studies may allow for safety profiling and potential use for patients with radiation retinopathy. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Retinal Diseases: An Update)
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