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Start Over Author "Canonica J" Topic complement factor h
2 results on '"Canonica J"'

1. CFH exerts anti-oxidant effects on retinal pigment epithelial cells independently from protecting against membrane attack complex.

Author

Borras C, Canonica J, Jorieux S, Abache T, El Sanharawi M, Klein C, Delaunay K, Jonet L, Salvodelli M, Naud MC, Arsenijevic Y, Shalabi A, Souchaud L, Behar-Cohen F, and Dinet V

Subjects
Aldehydes pharmacology, Apoptosis drug effects, Blotting, Western, Caspases metabolism, Cell Death drug effects, Cell Line, Complement Membrane Attack Complex metabolism, Humans, Induced Pluripotent Stem Cells drug effects, Induced Pluripotent Stem Cells metabolism, Microscopy, Electron, Transmission, Oxidative Stress drug effects, Real-Time Polymerase Chain Reaction, Recombinant Proteins, Retinal Pigment Epithelium metabolism, Tight Junctions drug effects, Complement Factor H pharmacology, Complement Membrane Attack Complex drug effects, Retinal Pigment Epithelium drug effects
Abstract

Age Related Macular Degeneration (AMD) is the first cause of social blindness in people aged over 65 leading to atrophy of retinal pigment epithelial cells (RPE), photoreceptors and choroids, eventually associated with choroidal neovascularization. Accumulation of undigested cellular debris within RPE cells or under the RPE (Drusen), oxidative stress and inflammatory mediators contribute to the RPE cell death. The major risk to develop AMD is the Y402H polymorphism of complement factor H (CFH). CFH interacting with oxidized phospholipids on the RPE membrane modulates the functions of these cells, but the exact role of CFH in RPE cell death and survival remain poorly understood. The aim of this study was to analyze the potential protective mechanism of CFH on RPE cells submitted to oxidative stress. Upon exposure to oxidized lipids 4-HNE (4-hydroxy-2-nonenal) derived from photoreceptors, both the human RPE cell line ARPE-19 and RPE cells derived from human induced pluripotent stem cells were protected from death only in the presence of the full length human recombinant CFH in the culture medium. This protective effect was independent from the membrane attack complex (MAC) formation. CFH maintained RPE cells tight junctions' structure and regulated the caspase dependent apoptosis process. These results demonstrated the CFH anti-oxidative stress functions independently of its capacity to inhibit MAC formation.

Published
2019
Full Text
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2. CFH exerts anti-oxidant effects on retinal pigment epithelial cells independently from protecting against membrane attack complex

Author

Borras, C., Canonica, J., Jorieux, S., Abache, T., El Sanharawi, M., Klein, C., Delaunay, K., Jonet, L., Salvodelli, M., Naud, M.C., Arsenijevic, Y., Shalabi, A., Souchaud, L., Behar-Cohen, F., Dinet, V., Centre de Recherche des Cordeliers (CRC (UMR_S_1138 / U1138)), École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Université de Paris (UP), Sorbonne Université (SU), Université de Paris - UFR Médecine Paris Centre [Santé] (UP Médecine Paris Centre), Université de Paris (UP), Université de Lausanne (UNIL), Universitätsklinikum Frankfurt, École pratique des hautes études (EPHE)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Laboratoire Français du fractionnement et des Biotechnologies, Centre de recherche du CEA/DSV/iBiTec-S/SIMOPRO, Développement, vieillissement et pathologie de la rétine, Institut National de la Santé et de la Recherche Médicale (INSERM), Physiopathologie des Maladies Oculaires : Innovations Therapeutiques, Université Pierre et Marie Curie - Paris 6 (UPMC)-IFR58-Institut National de la Santé et de la Recherche Médicale (INSERM), Unit of Retinal Degeneration and Regeneration, Laboratoire Angiogenèse et Micro-environnement des Cancers (LAMC), Université Sciences et Technologies - Bordeaux 1-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Paris Diderot - Paris 7 (UPD7), Laboratoire Français du Fractionnement et des Biotechnologies, and affiliation inconnue

Subjects
[SDV]Life Sciences [q-bio], Blotting, Western, Induced Pluripotent Stem Cells, lcsh:Medicine, Apoptosis, Complement Membrane Attack Complex, Retinal Pigment Epithelium, Real-Time Polymerase Chain Reaction, Article, Cell Line, Tight Junctions, Microscopy, Electron, Transmission, Humans, ddc:610, lcsh:Science, ComputingMilieux_MISCELLANEOUS, Aldehydes, Cell Death, lcsh:R, Recombinant Proteins, eye diseases, Complement cascade, Oxidative Stress, Caspases, Complement Factor H, lcsh:Q, sense organs, Visual system
Abstract

International audience; Age Related Macular Degeneration (AMD) is the first cause of social blindness in people aged over 65 leading to atrophy of retinal pigment epithelial cells (RPE), photoreceptors and choroids, eventually associated with choroidal neovascularization. Accumulation of undigested cellular debris within RPE cells or under the RPE (Drusen), oxidative stress and inflammatory mediators contribute to the RPE cell death. The major risk to develop AMD is the Y402H polymorphism of complement factor H (CFH). CFH interacting with oxidized phospholipids on the RPE membrane modulates the functions of these cells, but the exact role of CFH in RPE cell death and survival remain poorly understood. The aim of this study was to analyze the potential protective mechanism of CFH on RPE cells submitted to oxidative stress. Upon exposure to oxidized lipids 4-HNE (4-hydroxy-2-nonenal) derived from photoreceptors, both the human RPE cell line ARPE-19 and RPE cells derived from human induced pluripotent stem cells were protected from death only in the presence of the full length human recombinant CFH in the culture medium. This protective effect was independent from the membrane attack complex (MAC) formation. CFH maintained RPE cells tight junctions’ structure and regulated the caspase dependent apoptosis process. These results demonstrated the CFH anti-oxidative stress functions independently of its capacity to inhibit MAC formation.

Published
2019
Full Text
View/download PDF

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