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Editors Selection IGR 11-2

Basic research: C1q

Comment by Leonard A. Levin on:

13358 Longitudinal glaucoma screening for siblings of patients with primary open angle glaucoma: the Nottingham Family Glaucoma Screening Study, Sung VC; Koppens JM; Vernon SA et al., British Journal of Ophthalmology, 2006; 90: 59-63

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Stasi et al. (44) studied the expression of C1q, the first protein in the classic complement activation pathway, in

the retinas of DBA/2J mice, a murine glaucoma model. They found increased expression of mRNA (with reverse-transcription PCR) and protein (with immunoblotting and immunofluorescence) for C1q, with the levels increasing over time. It was localized to the Müller cells and near their end-feet. Preliminary studies of glaucomatous monkeys and humans showed similar histological findings. These results are interesting, because they raise the possibility that complement activation could be an effector arm in RGC death in glaucoma. Of course, it is also possible that increased C1q activation could be a result of glaucomatous RGC death, not a cause. Studies in C1q knock-out mice and analysis of C1q expression in other optic nerve injuries are presumably being considered by this expert team of investigators.

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