Title |
Deficiency of complement component 5 ameliorates glaucoma in DBA/2J mice
|
---|---|
Published in |
Journal of Neuroinflammation, June 2013
|
DOI | 10.1186/1742-2094-10-76 |
Pubmed ID | |
Authors |
Gareth R Howell, Ileana Soto, Margaret Ryan, Leah C Graham, Richard S Smith, Simon WM John |
Abstract |
Glaucoma is an age-related neurodegenerative disorder involving the loss of retinal ganglion cells (RGCs), which results in blindness. Studies in animal models have shown that activation of inflammatory processes occurs early in the disease. In particular, the complement cascade is activated very early in DBA/2J mice, a widely used mouse model of glaucoma. A comprehensive analysis of the role of the complement cascade in DBA/2J glaucoma has not been possible because DBA/2J mice are naturally deficient in complement component 5 (C5, also known as hemolytic complement, Hc), a key mediator of the downstream processes of the complement cascade, including the formation of the membrane attack complex. |
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Mendeley readers
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Demographic breakdown
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Researcher | 7 | 15% |
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