Abstract
Purpose: :
Purpose: Complement factor H is an important regulator of complement activation. Some single nucleotide polymorphisms in complement factor H are associated with an increased risk of AMD. It is thought that this may be due to a chronic increase in complement activation in the subretinal space. However, we would like to explore the role of Cfh in the more acute scenarios of choroidal neovascularization and light injury.
Methods: :
Methods: We are studying the development of choroidal neovascularization (CNV) using the laser injury model in 3-6 m old Cfh transgenic mice compared to age-matched B6 mice. ICAM-stained choroidal flat mounts were used to measure the size of CNV membranes. As a separate model of acute injury, we are also comparing the effect of intense/acute light injury in these two groups of mice. Fundus photography, light microscopy, RPE/choroid flat mounts and immunohistochemistry analysis were used to compare the response to light injury in Cfh transgenic vs. B6 mice.
Results: :
Results: The results of two separate laser injury experiments comparing CNV size in Cfh transgenic mice to B6 mice will be presented. We will also present the results of two separate light injury experiments comparing the fundus appearance, light microscopy changes, the number and type of macrophages, and the deposition of C3d in the retina/RPE/Bruch’s membrane/choroid of the Cfh transgenic vs. B6 mice.
Conclusions: :
Conclusions: The neovascular stage of AMD likely involves pathologic events that are different from those in the early stages of the disease. Although some epidemiologic studies suggest that Cfh may also be involved in this process, the data is not as compelling or consistent. We present data in our mouse model that may shed some light regarding the relevance of complement activation and complement factor H in acute injury and acute choroidal neovascularization.
Keywords: age-related macular degeneration • choroid: neovascularization • microglia