Intravitreal Injection of Amyloid β1-42 Activates the Complement System and Induces Retinal Inflammatory Responses and Malfunction in Mouse.

Abstract

To investigate whether intravitreal injection of amyloid β1-42 (Aβ1-42) activates the complement system and induces retinal inflammatory responses and malfunction, Aβ1-42 was applied intravitreally in mice. The expressions of key components of complement system were determined by real-time PCR. Retinal function was assessed by electroretinography. We found interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in Aβ1-42 treated mice retinas increased from day 1 to day 7. Compared with control group, mRNA expression of C1qa and C3 in the Aβ1-42 treated retinas increased at days 1 and 7. The level of CFB, CFD, or CFH increased at day 4 and day 7. Regulator of membrane attack complex (MAC), CD59a, increased from day 1 to day 7. The expression of the main complement components in Aβ1-42 treated eyes increased at days 4 and 7. Therefore, our results suggested that exogenous Aβ1-42 activated CP and AP of the complement system in mice retinas, induced retinal inflammatory responses, and caused retinal malfunction.