NDLI: Retinal Pigment Epithelial Cells Mitigate the Effects of Complement Attack by Endocytosis of C5b-9.

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Retinal Pigment Epithelial Cells Mitigate the Effects of Complement Attack by Endocytosis of C5b-9.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Greenwood, John Futter, Clare Moss, Stephen E. Burgoyne, Tom Lueck, Katharina Georgiannakis, Apostolos
Description	Country affiliation: United kingdom Author Affiliation: Georgiannakis A ( Department of Cell Biology, University College London Institute of Ophthalmology, London EC1V9EL, United Kingdom.); Burgoyne T ( Department of Cell Biology, University College London Institute of Ophthalmology, London EC1V9EL, United Kingdom.); Lueck K ( Department of Cell Biology, University College London Institute of Ophthalmology, London EC1V9EL, United Kingdom.); Futter C ( Department of Cell Biology, University College London Institute of Ophthalmology, London EC1V9EL, United Kingdom.); Greenwood J ( Department of Cell Biology, University College London Institute of Ophthalmology, London EC1V9EL, United Kingdom.); Moss SE ( Department of Cell Biology, University College London Institute of Ophthalmology, London EC1V9EL, United Kingdom s.moss@ucl.ac.uk.)
Abstract	Retinal pigment epithelial (RPE) cell death is a hallmark of age-related macular degeneration. The alternative pathway of complement activation is strongly implicated in RPE cell dysfunction and loss in age-related macular degeneration; therefore, it is critical that RPE cells use molecular strategies to mitigate the potentially harmful effects of complement attack. We show that the terminal complement complex C5b-9 assembles rapidly on the basal surface of cultured primary porcine RPE cells but disappears over 48 h without any discernable adverse effects on the cells. However, in the presence of the dynamin inhibitor dynasore, C5b-9 was almost completely retained at the cell surface, suggesting that, under normal circumstances, it is eliminated via the endocytic pathway. In support of this idea, we observed that C5b-9 colocalizes with the early endosome marker EEA1 and that, in the presence of protease inhibitors, it can be detected in lysosomes. Preventing the endocytosis of C5b-9 by RPE cells led to structural defects in mitochondrial morphology consistent with cell stress. We conclude that RPE cells use the endocytic pathway to prevent the accumulation of C5b-9 on the cell surface and that processing and destruction of C5b-9 by this route are essential for RPE cell survival.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1500937
Journal	The Journal of Immunology
Issue Number	7
Volume Number	195
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2015-10-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Complement Membrane Attack Complex Immunology Endocytosis Epithelial Cells Retinal Pigment Epithelium Animals Cell Membrane Metabolism Cells, Cultured Complement Activation Dynamins Antagonists & Inhibitors Cytology Hydrazones Pharmacology Macular Degeneration Pathology Mitochondria Protein Transport Swine Vesicular Transport Proteins Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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Retinal Pigment Epithelial Cells Mitigate the Effects of Complement Attack by Endocytosis of C5b-9

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Sub-lytic C5b-9 induces functional changes in retinal pigment epithelial cells consistent with age-related macular degeneration

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Dielectrophoretic characterization of peroxidized retinal pigment epithelial cells as a model of age-related macular degeneration

Retinal Pigment Epithelial Cells Mitigate the Effects of Complement Attack by Endocytosis of C5b-9.

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