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Molecular Mechanisms and Treatment of Retinopathy
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Molecular Mechanisms and Treatment of Retinopathy

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 (15 May 2023) | Viewed by 8752

Special Issue Editors

Dr. Dora Reglodi

E-Mail Website
Guest Editor
Department of Anatomy, MTA-PTE PACAP Research Team, Centre for Neuroscience, Szentagothai Research Centre, University of Pecs Medical School, Szigeti ut 12, H-7624 Pecs, Hungary
Interests: PACAP; apoptosis; inflammation; cellular protection; vip; secretin; glucagon
Special Issues, Collections and Topics in MDPI journals
Dr. Tamás Atlasz

E-Mail Website
Guest Editor
Department of Sportbiology, University of Pecs, 7624 Pecs, Hungary
Interests: sport sciences; neurodegeneration; obesity; retinal degeneration; neuroprotection; animal studies

Special Issue Information

Dear Colleagues, 

The retina is considered to be an extension of the central nervous system, as it develops from the diencephalon part of the prosencephalon. As such, it shares several features with the brain, and its neuronal population is similarly sensitive to several toxic agents and other degenerative processes. There are various forms of retinopathies, including one of the leading cause of visual impairment, diabetic retinopathy. The molecular mechanisms of retinopathies are continuously being elucidated with inflammatory, apoptotic processes, and oxidative stress in focus. A lot of recent data shed light on mechanisms with the help of in vitro experiments with different retinal cell lines and animal models. Retinopathy models are also useful in drug development against the different forms of retinopathies. The aim of this Special Issue is to gather and review novel experimental research data on the molecular mechanisms and possible treatment strategies in retinopathies.

Dr. Dora Reglodi
Dr. Tamás Atlasz
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.

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Keywords

  • retinopathy
  • molecular mechanism
  • inflammation
  • apoptosis
  • cellular protection
  • oxidative stress

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Published Papers (3 papers)

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Research

14 pages, 7057 KiB  
Article
Protective Effects of Pituitary Adenylate-Cyclase-Activating Polypeptide on Retinal Vasculature and Molecular Responses in a Rat Model of Moderate Glaucoma
by Evelin Patko, Edina Szabo, Alexandra Vaczy, Dorottya Molitor, Eniko Tari, Lina Li, Adrienne Csutak, Gabor Toth, Dora Reglodi and Tamas Atlasz
Int. J. Mol. Sci. 2023, 24(17), 13256; https://doi.org/10.3390/ijms241713256 - 26 Aug 2023
Cited by 6 | Viewed by 1550
Abstract
Despite the high probability of glaucoma-related blindness, its cause is not fully understood and there is no efficient therapeutic strategy for neuroprotection. Vascular factors have been suggested to play an important role in glaucoma development and progression. Previously, we have proven the neuroprotective [...] Read more.
Despite the high probability of glaucoma-related blindness, its cause is not fully understood and there is no efficient therapeutic strategy for neuroprotection. Vascular factors have been suggested to play an important role in glaucoma development and progression. Previously, we have proven the neuroprotective effects of pituitary adenylate-cyclase-activating polypeptide (PACAP) eye drops in an inducible, microbeads model in rats that is able to reproduce many clinically relevant features of human glaucoma. In the present study, we examined the potential protective effects of PACAP1-38 on the retinal vasculature and the molecular changes in hypoxia. Ocular hypertension was induced by injection of microbeads into the anterior chamber, while control rats received PBS. PACAP dissolved in vehicle (1 µg/drop) or vehicle treatment was started one day after the injections for four weeks three times a day. Retinal degeneration was assessed with optical coherence tomography (OCT), and vascular and molecular changes were assessed by immunofluorescence labeling. HIF1-α and VEGF-A protein levels were measured by Western blot. OCT images proved severe retinal degeneration in the glaucomatous group, while PACAP1-38 eye drops had a retinoprotective effect. Vascular parameters were deteriorated and molecular analysis suggested hypoxic conditions in glaucoma. PACAP treatment exerted a positive effect against these alterations. In summary, PACAP could prevent the severe damage to the retina and its vasculature induced by ocular hypertension in a microbeads model. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Treatment of Retinopathy)
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13 pages, 4545 KiB  
Article
Retinal Organoids from an AIPL1 CRISPR/Cas9 Knockout Cell Line Successfully Recapitulate the Molecular Features of LCA4 Disease
by Pedro R. L. Perdigão, Bethany Ollington, Hali Sai, Amy Leung, Almudena Sacristan-Reviriego and Jacqueline van der Spuy
Int. J. Mol. Sci. 2023, 24(6), 5912; https://doi.org/10.3390/ijms24065912 - 21 Mar 2023
Cited by 10 | Viewed by 3308
Abstract
Aryl hydrocarbon receptor-interacting protein-like 1 (AIPL1) is expressed in photoreceptors where it facilitates the assembly of phosphodiesterase 6 (PDE6) which hydrolyses cGMP within the phototransduction cascade. Genetic variations in AIPL1 cause type 4 Leber congenital amaurosis (LCA4), which presents as rapid loss of [...] Read more.
Aryl hydrocarbon receptor-interacting protein-like 1 (AIPL1) is expressed in photoreceptors where it facilitates the assembly of phosphodiesterase 6 (PDE6) which hydrolyses cGMP within the phototransduction cascade. Genetic variations in AIPL1 cause type 4 Leber congenital amaurosis (LCA4), which presents as rapid loss of vision in early childhood. Limited in vitro LCA4 models are available, and these rely on patient-derived cells harbouring patient-specific AIPL1 mutations. While valuable, the use and scalability of individual patient-derived LCA4 models may be limited by ethical considerations, access to patient samples and prohibitive costs. To model the functional consequences of patient-independent AIPL1 mutations, CRISPR/Cas9 was implemented to produce an isogenic induced pluripotent stem cell line harbouring a frameshift mutation in the first exon of AIPL1. Retinal organoids were generated using these cells, which retained AIPL1 gene transcription, but AIPL1 protein was undetectable. AIPL1 knockout resulted in a decrease in rod photoreceptor-specific PDE6α and β, and increased cGMP levels, suggesting downstream dysregulation of the phototransduction cascade. The retinal model described here provides a novel platform to assess functional consequences of AIPL1 silencing and measure the rescue of molecular features by potential therapeutic approaches targeting mutation-independent pathogenesis. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Treatment of Retinopathy)
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19 pages, 2402 KiB  
Article
Proteomic Profiling Revealed Mitochondrial Dysfunction in Photoreceptor Cells under Hyperglycemia
by Christie Hang-I Lam, Jimmy Ka-Wai Cheung, Dennis Yan-Yin Tse and Thomas Chuen Lam
Int. J. Mol. Sci. 2022, 23(21), 13366; https://doi.org/10.3390/ijms232113366 - 1 Nov 2022
Cited by 9 | Viewed by 2812
Abstract
Diabetic retinopathy (DR) was identified as a leading cause of blindness and vision impairment in 2020. In addition to vasculopathy, DR has been found to involve retinal neurons, including amacrine cells and retinal ganglion cells. Despite possessing features that are susceptible to diabetic [...] Read more.
Diabetic retinopathy (DR) was identified as a leading cause of blindness and vision impairment in 2020. In addition to vasculopathy, DR has been found to involve retinal neurons, including amacrine cells and retinal ganglion cells. Despite possessing features that are susceptible to diabetic conditions, photoreceptor cells have received relatively little attention with respect to the development of DR. Until recently, studies have suggested that photoreceptors secret proinflammatory molecules and produce reactive oxygen species that contribute to the development of DR. However, the effect of hyperglycemia on photoreceptors and its underlying mechanism remains elusive. In this study, the direct effect of high glucose on photoreceptor cells was investigated using a 661w photoreceptor-like cell line. A data-independent sequential window acquisition of all theoretical mass spectra (SWATH)-based proteomic approach was employed to study changes induced by high glucose in the proteomic profile of the cells. The results indicated that high glucose induced a significant increase in apoptosis and ROS levels in the 661w cells, with mitochondrial dysfunction among the major affected canonical pathways. The involvement of mitochondrial dysfunction was further supported by increased mitochondrial fission and reduced mitochondrial bioenergetics. Collectively, these findings provide a biological basis for a possible role of photoreceptors in the pathogenesis of DR. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Treatment of Retinopathy)
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