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Antioxidants
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Multileveled Molecular Mechanisms Related to Oxidative Stress in Retinitis Pigmentosa
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Multileveled Molecular Mechanisms Related to Oxidative Stress in Retinitis Pigmentosa

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 November 2020) | Viewed by 21062

Special Issue Editors

Prof. Dr. Antonina Sidoti

E-Mail Website
Guest Editor
1. Università degli Studi di Messina, Messina, Italy
2. Istituto Euro-Mediterraneo di Scienza e Tecnologia (I.E.ME.S.T.), Palermo, Italy
Interests: genetics, genomics; cellular biology; 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
Dr. Luigi Donato

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,

As you know, Retinitis pigmentosa (RP) is a heterogeneous inherited ocular disorder. It is characterized by progressive retinal disruption with unusually complicated molecular genetic causes, the main cellular event causing the onset of retinitis pigmentosa in photoreceptor cells and rods and cones. Normally, photoreceptor cells survival is ensured by retinal pigment epithelium (RPE). Really, RPE provides many vital functions such as regulation of the visual cycle, metabolite transport and photoreceptor excitability, phagocytosis of photoreceptor outer segments, secretion of growth factors, and oxidative stress protection. Among the main causes of RP, there is the RPE disruption due to oxidative stress. RPE degeneration alters cell cycle, vesicular trafficking, cell migration, endoplasmic reticulum stress, chaperones activity, small GTPase signalling, retinoic acid cycle, microvascular integrity, chromosome stability, circadian rhythms, fatty acids metabolism, synapses integrity, and retinal cells rescue. This research topic will discuss 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

Manuscript Submission Information

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Keywords

  •  Oxidative stress
  •  Antioxidants
  •  Retinitis pigmentosa (RP)
  •  Retinal pigment epithelium (RPE)
  •  Photoreceptors
  •  Cellular death
  •  Apoptosis
  •  Autophagy
  •  Cellular metabolism
  •  Cell dycle
  •  Vesicular trafficking
  •  Cell migration
  •  Endoplasmic reticulum stress
  •  Chaperones activity
  •  Small GTPase signalling
  •  Retinoic Acid cycle
  •  Angiogenesis
  •  Microvascular integrity
  •  Chromosome stability
  •  Circadian rhythms
  •  Fatty acids metabolism
  •  Synapses integrity
  •  Retinal cells rescue.

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Published Papers (5 papers)

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Research

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17 pages, 1712 KiB  
Article
Expression of Pro-Angiogenic Markers Is Enhanced by Blue Light in Human RPE Cells
by Concetta Scimone, Simona Alibrandi, Sergio Zaccaria Scalinci, Edoardo Trovato Battagliola, Rosalia D’Angelo, Antonina Sidoti and Luigi Donato
Antioxidants 2020, 9(11), 1154; https://doi.org/10.3390/antiox9111154 - 20 Nov 2020
Cited by 53 | Viewed by 3381
Abstract
Inherited retinal dystrophies are characterized by photoreceptor death. Oxidative stress usually occurs, increasing vision loss, and oxidative damage is often reported in retinitis pigmentosa (RP). More than 300 genes have been reported as RP causing. In contrast, choroidal neovascularization (CNV) only occasionally develops [...] Read more.
Inherited retinal dystrophies are characterized by photoreceptor death. Oxidative stress usually occurs, increasing vision loss, and oxidative damage is often reported in retinitis pigmentosa (RP). More than 300 genes have been reported as RP causing. In contrast, choroidal neovascularization (CNV) only occasionally develops in the late stages of RP. We herein study the regulation of RP causative genes that are likely linked to CNV onset under oxidative conditions. We studied how the endogenous adduct N-retinylidene-N-retinylethanolamine (A2E) affects the expression of angiogenic markers in human retinal pigment epithelium (H-RPE) cells and a possible correlation with RP-causing genes. H-RPE cells were exposed to A2E and blue light for 3 and 6h. By transcriptome analysis, genes differentially expressed between A2E-treated cells and untreated ones were detected. The quantification of differential gene expression was performed by the Limma R package. Enrichment pathway analysis by the FunRich tool and gene prioritization by ToppGene allowed us to identify dysregulated genes involved in angiogenesis and linked to RP development. Two RP causative genes, AHR and ROM1, can be associated with an increased risk of CNV development. Genetic analysis of RP patients affected by CNV will confirm this hypothesis. Full article
(This article belongs to the Special Issue Multileveled Molecular Mechanisms Related to Oxidative Stress in Retinitis Pigmentosa)
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19 pages, 5373 KiB  
Article
Eucalyptol Inhibits Amyloid-β-Induced Barrier Dysfunction in Glucose-Exposed Retinal Pigment Epithelial Cells and Diabetic Eyes
by Dong Yeon Kim, Min-Kyung Kang, Eun-Jung Lee, Yun-Ho Kim, Hyeongjoo Oh, Soo-Il Kim, Su Yeon Oh, Woojin Na and Young-Hee Kang
Antioxidants 2020, 9(10), 1000; https://doi.org/10.3390/antiox9101000 - 15 Oct 2020
Cited by 14 | Viewed by 2926
Abstract
Hyperglycemia elicits tight junction disruption and blood-retinal barrier breakdown, resulting in diabetes-associated vison loss. Eucalyptol is a natural compound found in eucalyptus oil with diverse bioactivities. This study evaluated that eucalyptol ameliorated tight junctions and retinal barrier function in glucose/amyloid-β (Aβ)-exposed human retinal [...] Read more.
Hyperglycemia elicits tight junction disruption and blood-retinal barrier breakdown, resulting in diabetes-associated vison loss. Eucalyptol is a natural compound found in eucalyptus oil with diverse bioactivities. This study evaluated that eucalyptol ameliorated tight junctions and retinal barrier function in glucose/amyloid-β (Aβ)-exposed human retinal pigment epithelial (RPE) cells and in db/db mouse eyes. RPE cells were cultured in media containing 33 mM glucose or 5 μM Aβ for 4 days in the presence of 1–20 μM eucalyptol. The in vivo animal study employed db/db mice orally administrated with 10 mg/kg eucalyptol. Nontoxic eucalyptol inhibited the Aβ induction in glucose-loaded RPE cells and diabetic mouse eyes. Eucalyptol reversed the induction of tight junction-associated proteins of ZO-1, occludin-1 and matrix metalloproteinases in glucose- or Aβ-exposed RPE cells and in diabetic eyes, accompanying inhibition of RPE detachment from Bruch’s membrane. Adding eucalyptol to glucose- or Aβ-loaded RPE cells, and diabetic mouse eyes reciprocally reversed induction/activation of apoptosis-related bcl-2, bax, cytochrome C/Apaf-1 and caspases. Eucalyptol attenuated the generation of reactive oxygen species and the induction of receptor for advanced glycation end products in Aβ-exposed RPE cells and diabetic eyes. Eucalyptol may ameliorate RPE barrier dysfunction in diabetic eyes through counteracting Aβ-mediated oxidative stress-induced RPE cell apoptosis. Full article
(This article belongs to the Special Issue Multileveled Molecular Mechanisms Related to Oxidative Stress in Retinitis Pigmentosa)
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21 pages, 8490 KiB  
Article
Epigallocatechin Gallate Slows Retinal Degeneration, Reduces Oxidative Damage, and Modifies Circadian Rhythms in P23H Rats
by Lorena Perdices, Lorena Fuentes-Broto, Francisco Segura, Nicolás Cuenca, Elvira Orduna-Hospital and Isabel Pinilla
Antioxidants 2020, 9(8), 718; https://doi.org/10.3390/antiox9080718 - 8 Aug 2020
Cited by 18 | Viewed by 3278
Abstract
Retinitis pigmentosa (RP) includes a group of genetic disorders that involve the loss of visual function due to mutations mainly in photoreceptors but also in other retinal cells. Apoptosis, retinal disorganization, and inflammation are common in the progression of the disease. Epigallocatechin gallate [...] Read more.
Retinitis pigmentosa (RP) includes a group of genetic disorders that involve the loss of visual function due to mutations mainly in photoreceptors but also in other retinal cells. Apoptosis, retinal disorganization, and inflammation are common in the progression of the disease. Epigallocatechin gallate (EGCG) has been proved as beneficial in different eye diseases. Pigmented heterozygous P23H rat was used as an animal model of RP. Visual function was assessed by optomotor and electroretinogram (ERG) and circadian rhythms were evaluated by telemetry. Hepatic oxidative damage and antioxidant defenses were assessed using biochemical tests. The visual function of the EGCG P23H group was preserved, with a deterioration in the activity period and lower values in the interdaily stability parameter. Control rats treated with EGCG were less active than the sham group. EGCG increased antioxidant levels in P23H rats but reduced total hepatic antioxidant capacity by almost 42% in control rats compared to the sham group. We conclude that treatment with EGCG improves visual function and antioxidant status in P23H rats but diminishes antioxidant defenses in wild-type control animals, and slightly worsens activity circadian rhythms. Further studies are necessary to clarify the beneficial effects in disease conditions and in healthy organisms. Full article
(This article belongs to the Special Issue Multileveled Molecular Mechanisms Related to Oxidative Stress in Retinitis Pigmentosa)
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Review

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17 pages, 523 KiB  
Review
Molecular Mechanisms Related to Oxidative Stress in Retinitis Pigmentosa
by Carla Enrica Gallenga, Maria Lonardi, Sofia Pacetti, Sara Silvia Violanti, Paolo Tassinari, Francesco Di Virgilio, Mauro Tognon and Paolo Perri
Antioxidants 2021, 10(6), 848; https://doi.org/10.3390/antiox10060848 - 26 May 2021
Cited by 48 | Viewed by 6589
Abstract
Retinitis pigmentosa (RP) is an inherited retinopathy. Nevertheless, non-genetic biological factors play a central role in its pathogenesis and progression, including inflammation, autophagy and oxidative stress. The retina is particularly affected by oxidative stress due to its high metabolic rate and oxygen consumption [...] Read more.
Retinitis pigmentosa (RP) is an inherited retinopathy. Nevertheless, non-genetic biological factors play a central role in its pathogenesis and progression, including inflammation, autophagy and oxidative stress. The retina is particularly affected by oxidative stress due to its high metabolic rate and oxygen consumption as well as photosensitizer molecules inside the photoreceptors being constantly subjected to light/oxidative stress, which induces accumulation of ROS in RPE, caused by damaged photoreceptor’s daily recycling. Oxidative DNA damage is a key regulator of microglial activation and photoreceptor degeneration in RP, as well as mutations in endogenous antioxidant pathways involved in DNA repair, oxidative stress protection and activation of antioxidant enzymes (MUTYH, CERKL and GLO1 genes, respectively). Moreover, exposure to oxidative stress alters the expression of micro-RNA (miRNAs) and of long non-codingRNA (lncRNAs), which might be implicated in RP etiopathogenesis and progression, modifying gene expression and cellular response to oxidative stress. The upregulation of the P2X7 receptor (P2X7R) also seems to be involved, causing pro-inflammatory cytokines and ROS release by macrophages and microglia, contributing to neuroinflammatory and neurodegenerative progression in RP. The multiple pathways analysed demonstrate that oxidative microglial activation may trigger the vicious cycle of non-resolved neuroinflammation and degeneration, suggesting that microglia may be a key therapy target of oxidative stress in RP. Full article
(This article belongs to the Special Issue Multileveled Molecular Mechanisms Related to Oxidative Stress in Retinitis Pigmentosa)
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25 pages, 4889 KiB  
Review
Antioxidant and Biological Properties of Mesenchymal Cells Used for Therapy in Retinitis Pigmentosa
by Paolo Giuseppe Limoli, Enzo Maria Vingolo, Celeste Limoli and Marcella Nebbioso
Antioxidants 2020, 9(10), 983; https://doi.org/10.3390/antiox9100983 - 13 Oct 2020
Cited by 13 | Viewed by 3762
Abstract
Both tissue repair and regeneration are a priority in regenerative medicine. Retinitis pigmentosa (RP), a complex retinal disease characterized by the progressive loss of impaired photoreceptors, is currently lacking effective therapies: this represents one of the greatest challenges in the field of ophthalmological [...] Read more.
Both tissue repair and regeneration are a priority in regenerative medicine. Retinitis pigmentosa (RP), a complex retinal disease characterized by the progressive loss of impaired photoreceptors, is currently lacking effective therapies: this represents one of the greatest challenges in the field of ophthalmological research. Although this inherited retinal dystrophy is still an incurable genetic disease, the oxidative damage is an important pathogenetic element that may represent a viable target of therapy. In this review, we summarize the current neuroscientific evidence regarding the effectiveness of cell therapies in RP, especially those based on mesenchymal cells, and we focus on their therapeutic action: limitation of both oxidative stress and apoptotic processes triggered by the disease and promotion of cell survival. Cell therapy could therefore represent a feasible therapeutic option in RP. Full article
(This article belongs to the Special Issue Multileveled Molecular Mechanisms Related to Oxidative Stress in Retinitis Pigmentosa)
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