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Complement regulatory protein CD46 protects against choroidal neovascularization in mice
Valeriy Lyzogubov1, Xiaobo Wu2, Purushottam Jha1
1Department of Ophthalmology, Pat and Willard Walker Eye Research Center, Jones Eye Institute, University of Arkansas for Medical Sciences, Little Rock, Arkansas.
The American Journal of Pathology
|July 15, 2014
Summary
The complement regulator CD46 is present in the mouse eye and protects against choroidal neovascularization (CNV). CD46 deficiency increases susceptibility to experimental CNV due to complement dysregulation.
Area of Science:
- Ophthalmology
- Immunology
- Complement System Biology
Background:
- Complement system dysregulation is implicated in age-related macular degeneration.
- CD46, a complement regulator, is ubiquitously expressed in humans but was thought to be restricted to spermatozoa in mice.
- The role of CD46 in ocular tissues and its impact on neovascularization remain unclear.
Purpose of the Study:
- To investigate CD46 expression in the mouse eye.
- To determine the role of CD46 in experimental choroidal neovascularization (CNV).
- To explore the link between CD46, complement activation, and VEGF in the context of CNV.
Main Methods:
- Detection of CD46 mRNA and protein in posterior ocular segments of wild-type (WT) C57BL/6J mice.
- Analysis of membrane attack complex (MAC) and vascular endothelial growth factor (VEGF) levels in Cd46(-/-) knockout mice.
- Assessment of susceptibility to laser-induced CNV in WT and Cd46(-/-) mice, quantifying positive spots and lesion size over time.
Main Results:
- CD46 mRNA and protein were detected in the retina, retinal pigment epithelium, and choroid of WT mice.
- Cd46(-/-) mice showed elevated MAC and VEGF levels in the retina and choroid.
- Cd46(-/-) mice exhibited significantly increased susceptibility to laser-induced CNV, with higher incidence and larger lesion sizes compared to WT mice.
Conclusions:
- CD46 is expressed in the posterior segment of the mouse eye.
- CD46 plays a protective role against laser-induced choroidal neovascularization.
- CD46 deficiency exacerbates experimental CNV, likely due to impaired complement inhibition leading to increased MAC deposition and VEGF expression.
