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9. Fibrotic Changes in Rhegmatogenous Retinal Detachment.

Author

Harju, Niina, Kauppinen, Anu, and Loukovaara, Sirpa

Subjects
*NEUROGLIA, *PROLIFERATIVE vitreoretinopathy, *EXTRACELLULAR matrix, *RETINAL detachment, *CELL migration, *WOUND healing
Abstract

Rhegmatogenous retinal detachment (RRD) is a sight-threatening condition involving retinal detachment and the accumulation of fluid in the subretinal space. Proliferative vitreoretinopathy (PVR) is a pathologic complication that develops after RRD surgery, and approximately 5–10% of RRD cases develop post-operative PVR. Prolonged inflammation in the wound healing process, epithelial–mesenchymal transition (EMT), retinal pigment epithelial (RPE) cell migration and proliferation, and epiretinal, intraretinal, and subretinal fibrosis are typical in the formation of PVR. RPE cells undergo EMT and become fibroblast-like cells that migrate to the retina and vitreous, promoting PVR formation. Fibroblasts transform into myofibroblasts, which promote fibrosis by overproducing the extracellular matrix (ECM). RPE cells, fibroblasts, glial cells, macrophages, T lymphocytes, and increased ECM production form contractile epiretinal membranes. Cytokine release, complement activation, RPE cells, glial cells, and endothelial cells are all involved in retinal immune responses. Normally, wounds heal within 4 to 6 weeks, including hemostasis, inflammation, proliferation, and remodeling phases. Properly initiated inflammation, complement activation, and the function of neutrophils and glial cells heal the wound in the first stage. In a retinal wound, glial cells proliferate and fill the injured area. Gliosis tries to protect the neurons and prevent damage, but it becomes harmful when it causes scarring. If healing is complicated, prolonged inflammation leads to pathological fibrosis. Currently, there is no preventive treatment for the formation of PVR, and it is worth studying in the future. [ABSTRACT FROM AUTHOR]

Published
2025
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13. Metformin Alleviates Inflammation and Induces Mitophagy in Human Retinal Pigment Epithelium Cells Suffering from Mitochondrial Damage.

Author

Toppila, Maija, Ranta-aho, Sofia, Kaarniranta, Kai, Hytti, Maria, and Kauppinen, Anu

Subjects
MACULAR degeneration, REACTIVE oxygen species, CELL survival, CHROMATOPHORES, WESTERN immunoblotting, RHODOPSIN
Abstract

Mitochondrial malfunction, excessive production of reactive oxygen species (ROS), deficient autophagy/mitophagy, and chronic inflammation are hallmarks of age-related macular degeneration (AMD). Metformin has been shown to activate mitophagy, alleviate inflammation, and lower the odds of developing AMD. Here, we explored the ability of metformin to activate mitophagy and alleviate inflammation in retinal pigment epithelium (RPE) cells. Human ARPE-19 cells were pre-treated with metformin for 1 h prior to exposure to antimycin A (10 µM), which induced mitochondrial damage. Cell viability, ROS production, and inflammatory cytokine production were measured, while autophagy/mitophagy proteins were studied using Western blotting and immunocytochemistry. Metformin pre-treatment reduced the levels of proinflammatory cytokines IL-6 and IL-8 to 42% and 65% compared to ARPE-19 cells exposed to antimycin A alone. Metformin reduced the accumulation of the autophagy substrate SQSTM1/p62 (43.9%) and the levels of LC3 I and II (51.6% and 48.6%, respectively) after antimycin A exposure. Metformin also increased the colocalization of LC3 with TOM20 1.5-fold, suggesting active mitophagy. Antimycin A exposure increased the production of mitochondrial ROS (226%), which was reduced by the metformin pre-treatment (84.5%). Collectively, metformin showed anti-inflammatory and antioxidative potential with mitophagy induction in human RPE cells suffering from mitochondrial damage. [ABSTRACT FROM AUTHOR]

Published
2024
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21. Loss of NRF-2 and PGC-1α genes leads to retinal pigment epithelium damage resembling dry age-related macular degeneration

Author

Felszeghy, Szabolcs, Viiri, Johanna, Paterno, Jussi J., Hyttinen, Juha M.T., Koskela, Ali, Chen, Mei, Leinonen, Henri, Tanila, Heikki, Kivinen, Niko, Koistinen, Arto, Toropainen, Elisa, Amadio, Marialaura, Smedowski, Adrian, Reinisalo, Mika, Winiarczyk, Mateusz, Mackiewicz, Jerzy, Mutikainen, Maija, Ruotsalainen, Anna-Kaisa, Kettunen, Mikko, Jokivarsi, Kimmo, Sinha, Debasish, Kinnunen, Kati, Petrovski, Goran, Blasiak, Janusz, Bjørkøy, Geir, Koskelainen, Ari, Skottman, Heli, Urtti, Arto, Salminen, Antero, Kannan, Ram, Ferrington, Deborah A., Xu, Heping, Levonen, Anna-Liisa, Tavi, Pasi, Kauppinen, Anu, and Kaarniranta, Kai

Published
2019
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