Multileveled Molecular Mechanisms Related to Oxidative Stress in Retinitis Pigmentosa II

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (30 April 2022) | Viewed by 2638

Special Issue Editors


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Guest Editor
Department of Biomedical and Dental Sciences and Morphofunctional Imaging, Division of Medical Biotechnologies and Preventive Medicine, University of Messina, Via Consolare Valeria 1, 98125 Messina, Italy
Interests: rare genetic diseases such as cerebral cavernous malformations (CCMs); trimethylaminuria (TMAU) inherited retinal dystrophies (IRDs); retinitis pigmentosa (RP)
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E-Mail Website
Guest Editor
Department of Biomedical, Dental, Morphological and Functional Imaging Sciences, University of Messina, 98125 Messina, Italy
Interests: genetics, genomics; cellular biology; bioinformatics; next-generation sequencing (NGS); oxidative stress; inherited retinal dystrophies (IRDs); retinitis pigmentosa (RP); cerebral cavernous malformations (CCMs); trimethylaminuria (TMAU)
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We invite you to the second volume of this Special Issue entitled “Multileveled Molecular Mechanisms Related to Oxidative Stress in Retinitis Pigmentosa”. With the first volume, we reached a high translational impact from research results on novel biomarkers and innovative therapies acting on oxidative stress related to the very heterogeneous inherited ocular disorder group of Retinitis pigmentosa (RP). Even if the main cellular event determining the onset of retinitis pigmentosa is photoreceptor death, the molecular genetic causes remain unusually complicated. Generally, photoreceptor cell survival is ensured by retinal pigment epithelium (RPE), which provides many vital functions, such as phagocytosis of photoreceptor outer segments, metabolite transport, photoreceptor excitability, regulation of the visual cycle, secretion of growth factors, and oxidative stress protection. Among the main causes of RP, the RPE disruption induced by oxidative stress represents the most complex and still not sufficiently explored. RPE degeneration alters cell cycle, vesicular trafficking, cell migration, endoplasmic reticulum stress, chaperones activity, small GTPase signaling, retinoic acid cycle, microvascular integrity, chromosome stability, circadian rhythms, fatty acid metabolism, synapses integrity, and retinal cell rescue. This research topic will discuss the most recent preclinical and clinical evidence highlighting the central role of oxidative stress in the onset and progression of RP, analyzing the extraordinary complexity of the multileveled molecular mechanisms and the current strategies adopted to protect the retina.

Prof. Dr. Antonina Sidoti
Dr. Luigi Donato
Guest Editors

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Keywords

  • Oxidative stress
  • Antioxidants
  • Retinitis pigmentosa (RP)
  • Retinal pigment epithelium (RPE)
  • Photoreceptors
  • Cellular death
  • Apoptosis
  • Autophagy
  • Cellular metabolism
  • Cell cycle
  • Vesicular trafficking
  • Cell migration
  • Endoplasmic reticulum stress
  • Chaperone activity
  • Small GTPase signaling
  • Retinoic acid cycle
  • Angiogenesis
  • Microvascular integrity
  • Chromosome stability
  • Circadian rhythms
  • Fatty acid metabolism
  • Synapse integrity
  • Retinal cell rescue
  • Editome
  • Cellular biomarkers
  • RNAome

Published Papers (1 paper)

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Research

22 pages, 4689 KiB  
Article
Epitranscriptome Analysis of Oxidative Stressed Retinal Epithelial Cells Depicted a Possible RNA Editing Landscape of Retinal Degeneration
by Luigi Donato, Concetta Scimone, Simona Alibrandi, Sergio Zaccaria Scalinci, Carmela Rinaldi, Rosalia D’Angelo and Antonina Sidoti
Antioxidants 2022, 11(10), 1967; https://doi.org/10.3390/antiox11101967 - 30 Sep 2022
Cited by 34 | Viewed by 2088
Abstract
Oxidative stress represents one of the principal causes of inherited retinal dystrophies, with many related molecular mechanisms still unknown. We investigated the posttranscriptional RNA editing landscape of human retinal pigment epithelium cells (RPE) exposed to the oxidant agent N-retinylidene-N-retinyl ethanolamine (A2E) for 1 [...] Read more.
Oxidative stress represents one of the principal causes of inherited retinal dystrophies, with many related molecular mechanisms still unknown. We investigated the posttranscriptional RNA editing landscape of human retinal pigment epithelium cells (RPE) exposed to the oxidant agent N-retinylidene-N-retinyl ethanolamine (A2E) for 1 h, 2 h, 3 h and 6 h. Using a transcriptomic approach, refined with a specific multialgorithm pipeline, 62,880 already annotated and de novo RNA editing sites within about 3000 genes were identified among all samples. Approximately 19% of these RNA editing sites were found within 3′ UTR, including sites common to all time points that were predicted to change the binding capacity of 359 miRNAs towards 9654 target genes. A2E exposure also determined significant gene expression differences in deaminase family ADAR, APOBEC and ADAT members, involved in canonical and tRNA editing events. On GO and KEGG enrichment analyses, genes that showed different RNA editing levels are mainly involved in pathways strongly linked to a possible neovascularization of retinal tissue, with induced apoptosis mediated by the ECM and surface protein altered signaling. Collectively, this work demonstrated dynamic RNA editome profiles in RPE cells for the first time and shed more light on new mechanisms at the basis of retinal degeneration. Full article
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