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Antioxidants
Special Issues
Retinal Pigment Epithelial Dysfunction in Macular Degeneration and Therapeutic Interventions
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Retinal Pigment Epithelial Dysfunction in Macular Degeneration and Therapeutic Interventions

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 (7 August 2023) | Viewed by 4671

Special Issue Editors

Prof. Dr. Ram Kannan

E-Mail Website
Guest Editor
Doheny Eye Institute, 150 North Orange Grove Blvd., Pasadena, CA 91103, USA
Interests: oxidative stress; antioxidant defense; membrane transporters; mitochondrial function; retinal pigment epithelium; age-related macular degeneration (AMD); senescence; nanotherapy
Dr. Parameswaran G. Sreekumar

E-Mail Website
Guest Editor
Doheny Eye Institute, 150 North Orange Grove Blvd., Pasadena, CA 91103, USA
Interests: mitochondria; RPE senescence; small heat shock proteins; models of AMD; peptide therapy; lipid metabolism; inflammation

Special Issue Information

Dear Colleagues,

Age-related macular degeneration (AMD), the leading cause of irreversible visual loss in the elderly, is complicated by two blinding late forms of the disease: choroidal neovascularization (CNV) and geographic atrophy (GA or atrophic AMD). The retinal pigment epithelium (RPE), which is well positioned between the Bruch membrane and the photoreceptors, performs a variety of tasks including light absorption, epithelial transport, spatial ion buffering, the visual cycle, phagocytosis, secretion, and immunological regulation. Therefore, the RPE must function properly to preserve retinal health, and RPE dysfunction can manifest in retinal disorders such as AMD. Oxidative stress to mitochondria is an important contributory factor to cell death.  In addition to being signaling hubs for autophagy and inflammatory responses, mitochondria are involved in other areas of cellular activity.  The role of RPE in the pathogenic mechanisms of AMD, as well as interventional therapeutic strategies to ameliorate the disease, can be investigated using a variety of experimental models.

A research article or review on any subject related to RPE metabolism, mitochondrial homeostasis, inflammation, or the crosstalk with cellular organelles is welcome to the Special Issue.  Studies on antioxidants and related factors in in vitro and in vivo models of AMD are also among the interesting topics.

Prof. Dr. Ram Kannan
Dr. Parameswaran G. Sreekumar
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. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). 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.

Keywords

  • RPE
  • AMD
  • oxidative stress
  • antioxidants
  • mitochondrial dysfunction
  • autophagy
  • inflammation
  • neovascularization
  • targeted therapy

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Published Papers (2 papers)

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Research

20 pages, 4282 KiB  
Article
Endothelial Notch Signaling Regulates the Function of the Retinal Pigment Epithelial Barrier via EC Angiocrine Signaling
by Yali Niu, Yixuan Xi, Yutong Jing, Ziyi Zhou, Xiaojia Sun, Guoheng Zhang, Tianhao Yuan, Tianfang Chang and Guorui Dou
Antioxidants 2023, 12(11), 1979; https://doi.org/10.3390/antiox12111979 - 7 Nov 2023
Viewed by 1692
Abstract
The outer blood–retina barrier (oBRB), comprises tightly connected retinal pigment epithelium (RPE) cells, Bruch’s membrane, and choroid blood vessels, and is essential for retinal health and normal visual function. Disruption of the RPE barrier and its dysfunction can lead to retinal disorders such [...] Read more.
The outer blood–retina barrier (oBRB), comprises tightly connected retinal pigment epithelium (RPE) cells, Bruch’s membrane, and choroid blood vessels, and is essential for retinal health and normal visual function. Disruption of the RPE barrier and its dysfunction can lead to retinal disorders such as age-related macular degeneration (AMD). In the present study, we investigated the essential role of choroid endothelial cells (ECs) in the RPE barrier formation process and its dysfunction. We discovered that ECs promoted RPE barrier formation through angiocrine signaling. Through blocking or activating endothelial Notch signaling and conducting experiments in vitro and in vivo, we confirmed that endothelial Notch signaling regulated the expression of heparin-binding epidermal growth factor (HBEGF) and consequently impacted the expression and activity of matrix metalloproteinases (MMP)-9 in RPE cells. This modulation influenced the RPE extracellular matrix deposition, tight junctions and RPE barrier function. In in vivo experiments, the intravitreal administration of recombinant HBEGF (r-HBEGF) alleviated the RPE barrier disruption induced by subretinal injection (SI) or laser treatment and also rescued RPE barrier disruption in endothelial Notch-deficient mice. Our results showed that the endothelial Notch signaling drove HBEGF expression through angiocrine signaling and effectively improved RPE barrier function by regulating the MMP-9 expression in RPE cells. It suggests that the modulation of Notch signaling in the choroidal endothelium may offer a novel therapeutic strategy for retinal degenerative diseases. Full article
(This article belongs to the Special Issue Retinal Pigment Epithelial Dysfunction in Macular Degeneration and Therapeutic Interventions)
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17 pages, 5085 KiB  
Article
Paraoxonase 2 Deficiency Causes Mitochondrial Dysfunction in Retinal Pigment Epithelial Cells and Retinal Degeneration in Mice
by Parameswaran Gangadharan Sreekumar, Feng Su, Christine Spee, Elise Hong, Ravikiran Komirisetty, Eduardo Araujo, Steven Nusinowitz, Srinivasa T. Reddy and Ram Kannan
Antioxidants 2023, 12(10), 1820; https://doi.org/10.3390/antiox12101820 - 30 Sep 2023
Cited by 3 | Viewed by 1982
Abstract
Although AMD is a complex disease, oxidative stress is a crucial contributor to its development, especially in view of the higher oxygen demand of the retina. Paraoxonase 2 (PON2) is a ubiquitously and constitutively expressed antioxidant protein that is found intracellularly associated with [...] Read more.
Although AMD is a complex disease, oxidative stress is a crucial contributor to its development, especially in view of the higher oxygen demand of the retina. Paraoxonase 2 (PON2) is a ubiquitously and constitutively expressed antioxidant protein that is found intracellularly associated with mitochondrial membranes and modulates mitochondrial ROS production and function. The contribution of PON2 to AMD has not been studied to date. In this study, we examined the role of PON2 in AMD utilizing both in vitro and in vivo models of AMD with emphasis on mitochondrial function. Mitochondrial localization and regulation of PON2 following oxidative stress were determined in human primary cultured retinal pigment epithelium (hRPE) cells. PON2 was knocked down in RPE cells using siRNA and mitochondrial bioenergetics were measured. To investigate the function of PON2 in the retina, WT and PON2-deficient mice were administered NaIO3 (20 mg/kg) intravenously; fundus imaging, optical coherence tomography (OCT), electroretinography (ERG) were conducted; and retinal thickness and cell death were measured and quantified. In hRPE, mitochondrial localization of PON2 increased markedly with stress. Moreover, a time-dependent regulation of PON2 was observed following oxidative stress, with an initial significant increase in expression followed by a significant decrease. Mitochondrial bioenergetic parameters (basal respiration, ATP production, spare respiratory capacity, and maximal respiration) showed a significant decrease with oxidative stress, which was further exacerbated in the absence of PON2. NaIO3 treatment caused significant retinal degeneration, retinal thinning, and reduced rod and cone function in PON2-deficient mice when compared to WT mice. The apoptotic cells and active caspase 3 significantly increased in PON2-deficient mice treated with NaIO3, when compared to WT mice. Our investigation demonstrates that deficiency of PON2 results in RPE mitochondrial dysfunction and a decline in retinal function. These findings imply that PON2 may have a beneficial role in retinal pathophysiology and is worthy of further investigation. Full article
(This article belongs to the Special Issue Retinal Pigment Epithelial Dysfunction in Macular Degeneration and Therapeutic Interventions)
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