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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Hoh Kam, Jaimie Lenassi, Eva Malik, Talat H. Pickering, Matthew C. Jeffery, Glen |
| Description | Country affiliation: United kingdom Author Affiliation: Hoh Kam J ( Institute of Ophthalmology, University College London, London, United Kingdom.) |
| Abstract | Complement component C3 is the central complement component and a key inflammatory protein activated in age-related macular degeneration (AMD). AMD is associated with genetic variation in complement proteins that results in enhanced activation of C3 through the complement alternative pathway. These include complement factor H (CFH), a negative regulator of C3 activation. Both C3 inhibition and/or CFH augmentation are potential therapeutic strategies in AMD. Herein, we examined retinal integrity in aged (12 months) mice deficient in both factors H and C3 (CFH(-/-).C3(-/-)), CFH alone (CFH(-/-)), or C3 alone (C3(-/-)), and wild-type mice (C57BL/6). Retinal function was assessed by electroretinography, and retinal morphological features were analyzed at light and electron microscope levels. Retinas were also stained for amyloid ß (Aß) deposition, inflammation, and macrophage accumulation. Contrary to expectation, electroretinograms of CFH(-/-).C3(-/-) mice displayed more severely reduced responses than those of other mice. All mutant strains showed significant photoreceptor loss and thickening of Bruch's membrane compared with wild-type C57BL/6, but these changes were greater in CFH(-/-).C3(-/-) mice. CFH(-/-).C3(-/-) mice had significantly more Aß on Bruch's membrane, fewer macrophages, and high levels of retinal inflammation than the other groups. Our data show that both uncontrolled C3 activation (CFH(-/-)) and complete absence of C3 (CFH(-/-).C3(-/-) and C3(-/-)) negatively affect aged retinas. These findings suggest that strategies that inhibit C3 in AMD may be deleterious. |
| File Format | HTM / HTML |
| ISSN | 00029440 |
| Issue Number | 2 |
| Volume Number | 183 |
| e-ISSN | 15252191 |
| Journal | The American Journal of Pathology |
| Language | English |
| Publisher | Elsevier (on behalf of the American Society for Investigative Pathology) |
| Publisher Date | 2013-08-01 |
| Publisher Place | United States |
| Access Restriction | One Nation One Subscription (ONOS) |
| Subject Keyword | Electroretinography Research Support, Non-u.s. Gov't Microscopy, Electron, Scanning Complement C3 Deficiency Mice, Inbred C57bl Amyloid Beta-peptides Retina Discipline Pathology Metabolism Complement Factor H Journal Article Physiopathology Mice, Knockout Retinal Pigment Epithelium Animals Etiology Ultrastructure Photoreceptor Cells, Vertebrate Physiology Mice Macular Degeneration Bruch Membrane Disease Models, Animal |
| Content Type | Text |
| Resource Type | Article |
| Subject | Pathology and Forensic Medicine |
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