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Open Access Research

670-nm light treatment reduces complement propagation following retinal degeneration

Matt Rutar12*, Riccardo Natoli123, Rizalyn Albarracin12, Krisztina Valter123 and Jan Provis123

Author Affiliations

1 The John Curtin School of Medical Research, College of Medicine, Biology and Environment, The Australian National University, Building 131, Garran Rd, Canberra, ACT 2601, Australia

2 ARC Centre of Excellence in Vision Science, The Australian National University, Canberra, ACT 2601, Australia

3 ANU Medical School, The Australian National University, Canberra, ACT 2601, Australia

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Journal of Neuroinflammation 2012, 9:257  doi:10.1186/1742-2094-9-257

Published: 26 November 2012

Abstract

Aim

Complement activation is associated with the pathogenesis of age-related macular degeneration (AMD). We aimed to investigate whether 670-nm light treatment reduces the propagation of complement in a light-induced model of atrophic AMD.

Methods

Sprague–Dawley (SD) rats were pretreated with 9 J/cm2 670-nm light for 3 minutes daily over 5 days; other animals were sham treated. Animals were exposed to white light (1,000 lux) for 24 h, after which animals were kept in dim light (5 lux) for 7 days. Expression of complement genes was assessed by quantitative polymerase chain reaction (qPCR), and immunohistochemistry. Counts were made of C3-expressing monocytes/microglia using in situ hybridization. Photoreceptor death was also assessed using outer nuclear layer (ONL) thickness measurements, and oxidative stress using immunohistochemistry for 4-hydroxynonenal (4-HNE).

Results

Following light damage, retinas pretreated with 670-nm light had reduced immunoreactivity for the oxidative damage maker 4-HNE in the ONL and outer segments, compared to controls. In conjunction, there was significant reduction in retinal expression of complement genes C1s, C2, C3, C4b, C3aR1, and C5r1 following 670 nm treatment. In situ hybridization, coupled with immunoreactivity for the marker ionized calcium binding adaptor molecule 1 (IBA1), revealed that C3 is expressed by infiltrating microglia/monocytes in subretinal space following light damage, which were significantly reduced in number after 670 nm treatment. Additionally, immunohistochemistry for C3 revealed a decrease in C3 deposition in the ONL following 670 nm treatment.

Conclusions

Our data indicate that 670-nm light pretreatment reduces lipid peroxidation and complement propagation in the degenerating retina. These findings have relevance to the cellular events of complement activation underling the pathogenesis of AMD, and highlight the potential of 670-nm light as a non-invasive anti-inflammatory therapy.