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Complement modulation in the retinal pigment epithelium rescues photoreceptor degeneration in a mouse model of Stargardt disease.

Proc Natl Acad Sci U S A.. 2017-04; 
Lenis TL, Sarfare S, Jiang Z, Lloyd MB, Bok D, Radu RA.
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...α-tubulin (T9026; Sigma-Aldrich), LC3 (L7543; Sigma-Aldrich), β-actin (A00702; Genscript),…

摘要

Recessive Stargardt macular degeneration (STGD1) is caused by mutations in the gene for the ABCA4 transporter in photoreceptor outer segments. STGD1 patients and Abca4-/- (STGD1) mice exhibit buildup of bisretinoid-containing lipofuscin pigments in the retinal pigment epithelium (RPE), increased oxidative stress, augmented complement activation and slow degeneration of photoreceptors. A reduction in complement negative regulatory proteins (CRPs), possibly owing to bisretinoid accumulation, may be responsible for the increased complement activation seen on the RPE of STGD1 mice. CRPs prevent attack on host cells by the complement system, and complement receptor 1-like protein y (CRRY) is an important CRP in mice... More

关键词

bisretinoids; complement system; gene therapy; recessive Stargardt macular degeneration; retinal pigment epithelium