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Cells
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Retinal Pigment Epithelial Cells in Age-Related Macular Degeneration
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Retinal Pigment Epithelial Cells in Age-Related Macular Degeneration

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

Deadline for manuscript submissions: 1 August 2025 | Viewed by 3715

Special Issue Editor

Dr. Sujoy Bhattacharya

E-Mail Website
Guest Editor
Department of Ophthalmology and Visual Sciences, Vanderbilt University Medical Center, Nashville, TN, USA
Interests: autophagy; mitophagy; epithelial–mesenchymal transition; macular dystrophies; geographic atrophy; iPSCs; mitochondria; RPE bioenergetics; gene networks

Special Issue Information

Dear Colleagues,

The biology of atrophic (dry) age-related macular degeneration (aAMD) and its progression to geographic atrophy (GA) is multifactorial and complex. In aAMD, the retinal pigment epithelium (RPE) begins to degenerate, causing irreversible vision loss. It is challenging to develop in vitro and in vivo disease models recapitulating critical features of AMD pathobiology. There are no current effective treatments for RPE cell loss in aAMD. Intriguing approaches to treating atrophic AMD include 1) understanding the mechanisms contributing to RPE degeneration in atrophic AMD, 2) developing therapies focused on stimulating RPE development and regeneration, and 3) patient iPSC-based RPE disease modeling for studying disease mechanisms and drug screening.

This Special Issue will examine novel regulators stimulating an intrinsic regenerative response in the mature RPE, methods to isolate and maintain RPE cells isolated from rodents and human donor eyes, age-related changes in RPE mitochondrial function, metabolic pathways, and extracellular matrix reorganization, transcriptomic and proteomic analyses of iPSC-derived RPE, and novel animal models recapitulating hallmarks of aAMD pathobiology.

Dr. Sujoy Bhattacharya
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

  • atrophic age-related macular degeneration
  • iPSC-derived RPE
  • animal models

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Published Papers (2 papers)

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Research

23 pages, 15424 KiB  
Article
Prominin-1 Knockdown Causes RPE Degeneration in a Mouse Model
by Sujoy Bhattacharya, Tzushan Sharon Yang, Bretton P. Nabit, Evan S. Krystofiak, Tonia S. Rex and Edward Chaum
Cells 2024, 13(21), 1761; https://doi.org/10.3390/cells13211761 - 24 Oct 2024
Viewed by 1853
Abstract
There are currently no effective treatments for retinal pigment epithelial (RPE) cell loss in atrophic AMD (aAMD). However, our research on Prominin-1 (Prom1), a known structural protein in photoreceptors (PRs), has revealed its distinct role in RPE and offers promising insights. [...] Read more.
There are currently no effective treatments for retinal pigment epithelial (RPE) cell loss in atrophic AMD (aAMD). However, our research on Prominin-1 (Prom1), a known structural protein in photoreceptors (PRs), has revealed its distinct role in RPE and offers promising insights. While pathogenic Prom1 mutations have been linked to macular diseases with RPE atrophy, the broader physiological impact of dysfunctional Prom1 in RPE loss is unclear. We have shown that Prom1 plays a crucial role in regulating autophagy and cellular homeostasis in human and mouse RPE (mRPE) cells in vitro. Nevertheless, a comprehensive understanding of its in vivo expression and function in mRPE remains to be elucidated. To characterize Prom1 expression in RPE in situ, we used RNAscope assays and immunogold electron microscopy (EM). Our use of chromogenic and fluorescent RNAscope assays in albino and C57BL/6J mouse retinal sections has revealed Prom1 mRNA expression in perinuclear regions in mRPE in situ. Immunogold EM imaging showed Prom1 expression in RPE cytoplasm and mitochondria. To confirm Prom1 expression in RPE, we interrogated human RPE single-cell RNA-sequencing datasets using an online resource, Spectacle. Our analysis showed Prom1 expression in human RPE. To investigate Prom1’s function in RPE homeostasis, we performed RPE-specific Prom1 knockdown (KD) using subretinal injections of AAV2/1.CMV.saCas9.U6.Prom1gRNA in male and female mice. Our data show that RPE-specific Prom1-KD in vivo resulted in abnormal RPE morphology, subretinal fluid accumulation, and secondary PR loss. These changes were associated with patchy RPE cell death and reduced a-wave amplitude, indicating retinal degeneration. Our findings underscore the central role of Prom1 in cell-autonomous mRPE homeostasis. The implications of Prom1-KD causing aAMD-like RPE defects and retinal degeneration in a mouse model are significant and could lead to novel treatments for aAMD. Full article
(This article belongs to the Special Issue Retinal Pigment Epithelial Cells in Age-Related Macular Degeneration)
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9 pages, 3790 KiB  
Communication
The Endogenous Expression of BMI1 in Adult Human Eyes
by Zhongyang Lu, Maria G. Morales, Shufeng Liu and Hema L. Ramkumar
Cells 2024, 13(19), 1672; https://doi.org/10.3390/cells13191672 - 9 Oct 2024
Viewed by 1222
Abstract
BMI1, also known as B lymphoma Mo-MLV insertion region 1, is a protein in the Polycomb group that is implicated in various cellular processes, including stem cell self-renewal and the regulation of cellular senescence. BMI1 plays a role in the regulation of retinal [...] Read more.
BMI1, also known as B lymphoma Mo-MLV insertion region 1, is a protein in the Polycomb group that is implicated in various cellular processes, including stem cell self-renewal and the regulation of cellular senescence. BMI1 plays a role in the regulation of retinal progenitor cells and the renewal of adult neuronal cells. However, the presence, location, and quantification of BMI1 in the adult human eye have never previously been reported. In this study, we collected 45 frozen globes from eye banks, and ocular tissues were dissected. Protein was quantified by utilizing a custom electrochemiluminescence (ECL) assay developed to quantify the BMI1 protein. BMI1 was found in all ocular tissues at the following levels: the retina (1483.6 ± 191.7 pg/mL) and the RPE (296.4 ± 78.1 pg/mL). BMI1 expression was noted ubiquitously in the GCL (ganglion cell layer), the INL (inner nuclear layer), the ONL (outer nuclear layer), and the RPE (retinal pigment epithelium) via immunofluorescence, with higher levels in the inner than in the outer retinal layers and the RPE. These data confirm that BMI1 is expressed in the human retina. Further studies will illuminate the role that BMI1 plays in ocular cells. BMI1 levels are lower in aged retinas, possibly reflecting changes in retinal somatic and stem cell maintenance and disease susceptibility. Full article
(This article belongs to the Special Issue Retinal Pigment Epithelial Cells in Age-Related Macular Degeneration)
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