Evaluation of CD59 as a Potential Therapy for AMD Complement-mediated damage to the retinal pigment epithelium (RPE), Bruch membrane, and choroid has been associated with pathogenesis in age-related macular degeneration (AMD). The final step of complement activation involves lysis of cells by the insertion of the membrane attack complex (MAC) in the cell membrane. The hypothesis that local overexpression of human CD59 (hCD59, also known as Protectin, a complement regulatory protein) delivered by an virus to mouse RPE cells protects those cells from MAC deposition and lysis was tested.

MAC deposition on mouse cells and murine ocular tissues including RPE and cornea was developed to permit testing of human complement regulators in mice. A recombinant adenovirus-expressing CD59 was generated, and this virus was injected into the subretinal space of adult mice.

The investigators found that CD59 does protect RPE, cornea, or cells in culture from MAC deposition and MAC-mediated damage.

The researchers conclude that MAC deposition on mouse ocular tissues allows testing of complement regulators that may have potential in the treatment of AMD or other diseases associated with complement activation.

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Investigative Ophthalmology and Visual Science. 2008;49:4126-4136.