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Eliminating complement factor D reduces photoreceptor susceptibility to light-induced damage
Bärbel Rohrer1, Yao Guo, Kannan Kunchithapautham
1Department of Neurosciences Division of Research, Medical University of South Carolina, Charleston, SC 29425, USA. rohrer@musc.edu
Insights
Eliminating the alternative complement pathway protects photoreceptors from light-induced degeneration. This suggests the complement system plays a key role in age-related macular degeneration pathogenesis.
Area of Science:
- Ophthalmology
- Immunology
- Neuroscience
Background:
- Age-related macular degeneration (AMD) is linked to genetic risk factors like complement factor H (CFH) and complement factor B (CFB).
- Inadequate control of complement-driven inflammation is hypothesized to be a major factor in AMD pathogenesis.
Purpose of the Study:
- To investigate the role of the complement system in oxidative stress-mediated photoreceptor degeneration.
- To test the involvement of complement factors in the light-damage mouse model.
Main Methods:
- Gene expression changes in BALB/c retinas after constant light (CL) exposure were analyzed using microarrays and real-time PCR.
- Photoreceptor degeneration susceptibility was assessed in complement factor D knockout (CFD(-/-)) mice.
- Electrophysiologic and histologic techniques were used to analyze eye tissues.
Main Results:
- Genes involved in complement activation were significantly upregulated following CL exposure.
- Altered gene profiles resembled proteins in drusen and genes found in AMD patients' retinas.
- CFD(-/-) mice showed significantly protected photoreceptors after CL challenge compared to controls.
Conclusions:
- Rod degeneration in CL-damaged retinas involves the alternative complement pathway.
- Eliminating the alternative complement pathway demonstrates neuroprotective effects.
- The light damage mouse model is suitable for studying complement-mediated photoreceptor degeneration.
Purpose:
Genetic risk factors such as variations in complement factors H (CFH) and B (CFB) have been implicated in the etiology of age-related macular degeneration. It has been hypothesized that inadequate control of complement-driven inflammation may be a major factor in disease pathogenesis. The authors tested the involvement of the complement system in an experimental model for oxidative stress-mediated photoreceptor degeneration, the light-damage mouse model.
Methods:
Changes in gene expression were assessed in BALB/c retinas in response to constant-light (CL) exposure using microarrays and real-time PCR. Susceptibility to CL exposure was tested in CFD(-/-) mice on a BALB/c background. Eyes were analyzed using electrophysiologic and histologic techniques.
Results:
Genes encoding for proteins involved in complement activation were significantly upregulated after CL. The altered gene profiles were similar to proteins accumulated in drusen and to genes identified in the retina and RPE/choroid of patients with age-related macular degeneration. Cyclic-light reared CFD(-/-) and CFD(+/+) mice had indistinguishable rod function and number; however, after CL challenge, CFD(-/-) photoreceptors were significantly protected.
Conclusions:
These results suggest that rod degeneration in the CL-damaged retina involves the activity of the alternative complement pathway and that eliminating the alternative pathway is neuroprotective. Thus, the light damage albino mouse model may be a good model to study complement-mediated photoreceptor degeneration.
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