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D. V. Pow, N. L. Barnett, J. M. Provis, S. M. Taylor, T. Woodruff, A. S. Kwan; Microhaemorrhage and Focal Expression of a Marker of the Complement Cascade in a Rat AMD Model. Invest. Ophthalmol. Vis. Sci. 2009;50(13):715.
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Rats that exhibit spontaneous microhaemorhages subsequently develop focal AMD-like lesions (Pow and Diaz 2007, IOVS 49:2790-8). After microhaemorrhage there is a requirement for focal clotting. There is an intimate functional linkage between the clotting system and the complement system, both of which are proteolytic cascades that derive from a common ancestral cascade. AMD is known to be associated with the focal activation of the complement cascade. Accordingly we have examined whether there is evidence for focal expression of the complement C5a receptor (which is a critical regulator of inflammation) after retinal microhaemorrhage.
Immunocytochemistry for the complement C5a receptor was performed on retinae from rats with prior microhaemorrhage.
We demonstrate focal expression of the C5a receptor at sites of prior microhaemorrhage.
Microhaemorrhage appears to induce expression of a critical component of the alternate complement pathway. As such it provides a plausible biochemical mechanism by which bleeding, including the bleeds that occur spontaneously in aged humans, could lead to focal activation of the complement cascade. In the absence of sufficient host cell protection, (perhaps due to complement factor-h polymorphisms), microhaemorrhage and consequent complement cascade activation could lead to focal neurodegeneration such as is observed in AMD.
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