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Cells
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Molecular and Cellular Basis of Retinal Diseases
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Molecular and Cellular Basis of Retinal Diseases

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (31 January 2023) | Viewed by 3965

Special Issue Editor

Dr. Menaka Thounaojam

E-Mail Website
Guest Editor
Department of Ophthalmology, Medical College of Georgia, Augusta University, Augusta, GA 30912, USA
Interests: miRNA; Retinopathy of prematurity; bile acid metabolism
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The onset and progression of various retinal diseases are associated with many abnormal molecular and cellular processes that affect retinal structure and function, resulting in the neural and vascular degeneration of the retina. Retinal cells have a variety of subcellular specializations that are functionally significant; hence, in various retinal diseases, one or more of these cells are compromised. In addition, retinal disease pathogenesis is influenced by oxidative stress, metabolic dysregulation, related inflammation, dysregulated immunological responses, potential blood–retinal barrier disruption, and tissue damage. Hence, identifying the molecular and cellular mechanisms responsible for these processes is crucial for the early diagnosis and prevention of these pathological outcomes to curb blindness, and remains the primary goal of vision researchers. Although recent experimental and clinical research has offered essential molecular evidence for a better understanding of retinal illnesses, future investigations will provide further insight into retinal pathogenesis and create new possibilities for diagnostics, biomarker creation, and pharmacological treatment. This Special Issue welcomes the submission of original research and review articles as well as clinical trials related to any cellular and molecular aspects of retinal diseases, the identification and exploration of novel targets, and the development and testing of novel therapies.

Dr. Menaka Thounaojam
Guest Editor

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. Cells is an international peer-reviewed open access semimonthly 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 2700 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

  • retinal degeneration
  • retinopathy of prematurity
  • diabetic retinopathy
  • age-related macular degeneration
  • retinal inflammation
  • therapeutic targets
  • biomarkers
  • oxidative stress
  • retinal metabolism

Published Papers (2 papers)

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Research

18 pages, 7734 KiB  
Article
IL-33 via PKCμ/PRKD1 Mediated α-Catenin Phosphorylation Regulates Endothelial Cell-Barrier Integrity and Ischemia-Induced Vascular Leakage
by Deepti Sharma, Geetika Kaur, Shivantika Bisen, Anamika Sharma, Ahmed S. Ibrahim and Nikhlesh K. Singh
Cells 2023, 12(5), 703; https://doi.org/10.3390/cells12050703 - 23 Feb 2023
Cited by 1 | Viewed by 1987
Abstract
Angiogenesis, neovascularization, and vascular remodeling are highly dynamic processes, where endothelial cell–cell adhesion within the vessel wall controls a range of physiological processes, such as growth, integrity, and barrier function. The cadherin–catenin adhesion complex is a key contributor to inner blood–retinal barrier (iBRB) [...] Read more.
Angiogenesis, neovascularization, and vascular remodeling are highly dynamic processes, where endothelial cell–cell adhesion within the vessel wall controls a range of physiological processes, such as growth, integrity, and barrier function. The cadherin–catenin adhesion complex is a key contributor to inner blood–retinal barrier (iBRB) integrity and dynamic cell movements. However, the pre-eminent role of cadherins and their associated catenins in iBRB structure and function is not fully understood. Using a murine model of oxygen-induced retinopathy (OIR) and human retinal microvascular endothelial cells (HRMVECs), we try to understand the significance of IL-33 on retinal endothelial barrier disruption, leading to abnormal angiogenesis and enhanced vascular permeability. Using electric cell-substrate impedance sensing (ECIS) analysis and FITC-dextran permeability assay, we observed that IL-33 at a 20 ng/mL concentration induced endothelial-barrier disruption in HRMVECs. The adherens junction (AJs) proteins play a prominent role in the selective diffusion of molecules from the blood to the retina and in maintaining retinal homeostasis. Therefore, we looked for the involvement of adherens junction proteins in IL-33-mediated endothelial dysfunction. We observed that IL-33 induces α-catenin phosphorylation at serine/threonine (Ser/Thr) residues in HRMVECs. Furthermore, mass-spectroscopy (MS) analysis revealed that IL-33 induces the phosphorylation of α-catenin at Thr654 residue in HRMVECs. We also observed that PKCμ/PRKD1-p38 MAPK signaling regulates IL-33-induced α-catenin phosphorylation and retinal endothelial cell-barrier integrity. Our OIR studies revealed that genetic deletion of IL-33 resulted in reduced vascular leakage in the hypoxic retina. We also observed that the genetic deletion of IL-33 reduced OIR-induced PKCμ/PRKD1-p38 MAPK-α-catenin signaling in the hypoxic retina. Therefore, we conclude that IL-33-induced PKCμ/PRKD1-p38 MAPK-α-catenin signaling plays a significant role in endothelial permeability and iBRB integrity. Full article
(This article belongs to the Special Issue Molecular and Cellular Basis of Retinal Diseases)
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12 pages, 1019 KiB  
Article
Exosomal miRNA Profiling in Vitreous Humor in Proliferative Diabetic Retinopathy
by Agnieszka Kot and Radoslaw Kaczmarek
Cells 2023, 12(1), 123; https://doi.org/10.3390/cells12010123 - 28 Dec 2022
Cited by 8 | Viewed by 1664
Abstract
MicroRNAs (miRNAs) are small noncoding RNAs which mediate some of the pathological mechanisms of diabetic retinopathy. The aim of this study was to identify differentially expressed miRNAs in the vitreal exosomes of proliferative diabetic retinopathy (PDR) patients and non-diabetic controls. Exosomes were extracted [...] Read more.
MicroRNAs (miRNAs) are small noncoding RNAs which mediate some of the pathological mechanisms of diabetic retinopathy. The aim of this study was to identify differentially expressed miRNAs in the vitreal exosomes of proliferative diabetic retinopathy (PDR) patients and non-diabetic controls. Exosomes were extracted from the vitreous samples of 10 PDR patients and 10 controls. The expression of 372 miRNAs was determined using a quantitative polymerase chain reaction (qPCR) panel. We have demonstrated a significant dysregulation in 26 miRNAs. The most remarkable findings include a profound attenuation of the miR-125 family, as well as enhanced miR-21-5p expression in the diabetic samples. We also showed the downregulation of miR-204-5p and the upregulation of let-7g in PDR compared to the controls. This study identified miR-125 and miR-21 as potential targets for further functional analysis regarding their putative role in the pathogenesis of PDR. Full article
(This article belongs to the Special Issue Molecular and Cellular Basis of Retinal Diseases)
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