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Retinal Pigment Epithelium and Müller Progenitor Cell Interaction Increase Müller Progenitor Cell Expression of
Gisela Velez1, Alexa R Weingarden, Budd A Tucker
1Department of Ophthalmology, University of Massachusetts Medical School, Worcester, MA 01605, USA.
Abstract:
Purpose. Proliferative vitreoretinopathy (PVR) is a complication of retinal detachment characterized by redetachment of the retina as a result of membrane formation and contraction. A variety of retinal cells, including retinal pigment epithelial (RPE) and Müller glia, and growth factors may be responsible. Platelet-derived growth factor receptor alpha (PDGFRα) is found in large quantities in PVR membranes, and is intrinsic to the development of PVR in rabbit models. This study explores the expression of PDGFR in cocultures of RPE and Müller cells over time to examine how these two cell types may collaborate in the development of PVR. We also examine how changes in PDGFRα expression alter Müller cell pathogenicity. Methods. Human MIO-M1 Müller progenitor (MPC) and ARPE19 cells were studied in a transmembrane coculture system. Immunocytochemistry and Western blot were used to look at PDGFRα, PDGFRβ, and GFAP expression. A transfected MPC line cell line expressing the PDGFRα (MIO-M1α) was generated, and tested in a rabbit model for its ability to induce PVR. Results. The expression of PDGFRα and PDGFRβ was upregulated in MIO-M1 MPCs cocultured with ARPE19 cells; GFAP was slightly decreased. Increased expression of PDGFRα in the MIO-M1 cell line resulted in increased pathogenicity and enhanced ability to induce PVR in a rabbit model. Conclusions. Müller and RPE cell interaction can lead to upregulation of PDGFRα and increased Müller cell pathogenicity. Müller cells may play a more active role than previously thought in the development of PVR membranes, particularly when stimulated by an RPE-cell-rich environment. Additional studies of human samples and in animal models are warranted.
Insights
Müller and retinal pigment epithelial (RPE) cells interact to increase Platelet-Derived Growth Factor Receptor alpha (PDGFRα) in proliferative vitreoretinopathy (PVR). This PDGFRα upregulation enhances Müller cell pathogenicity, contributing to retinal redetachment.
Area of Science:
- Ophthalmology
- Cell Biology
- Regenerative Medicine
Background:
- Proliferative vitreoretinopathy (PVR) is a severe complication of retinal detachment, leading to redetachment via membrane formation and contraction.
- Retinal pigment epithelial (RPE) cells and Müller glia are implicated in PVR pathogenesis, alongside growth factors.
- Platelet-derived growth factor receptor alpha (PDGFRα) is abundant in PVR membranes and crucial for PVR development in animal models.
Purpose of the Study:
- To investigate PDGFR expression in cocultures of RPE and Müller cells over time.
- To understand the collaborative role of RPE and Müller cells in PVR development.
- To assess how altered PDGFRα expression affects Müller cell pathogenicity.
Main Methods:
- Human MIO-M1 Müller progenitor cells (MPCs) and ARPE19 cells were cultured in a transmembrane system.
- Immunocytochemistry and Western blot analyzed PDGFRα, PDGFRβ, and GFAP expression.
- A MIO-M1 cell line overexpressing PDGFRα (MIO-M1α) was created and tested in a rabbit PVR model.
Main Results:
- Coculture of MIO-M1 MPCs with ARPE19 cells upregulated PDGFRα and PDGFRβ expression, with a slight decrease in GFAP.
- Increased PDGFRα expression in MIO-M1 cells enhanced their pathogenicity.
- The MIO-M1α cell line demonstrated an increased ability to induce PVR in a rabbit model.
Conclusions:
- Interaction between Müller and RPE cells upregulates PDGFRα, increasing Müller cell pathogenicity.
- Müller cells may play a more significant role in PVR membrane development than previously recognized, especially in RPE-rich environments.
- Further research using human samples and animal models is recommended to validate these findings.
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