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Updated: Sep 20, 2025
Isolation of Primary Mouse Retinal Pigmented Epithelium Cells
Published on: November 4, 2022
Complement C3 deficiency alleviates alkylation-induced retinal degeneration in mice
Lu Du1, Guang-Hua Peng2,3,4
1Department of Ophthalmology, Chinese PLA General Hospital, Beijing, 100039, China.
Background:
It has been found that the extensive use of anticancer drugs containing DNA-alkylating agents not only target cancer cells but also cause retinal inflammation through toxic intermediates. Complement C3 (C3) is a core component of the complement activation pathway, and dysregulation of the complement pathway is involved in several retinal degenerative diseases. However, whether C3 plays a critical role in alkylation-induced retinal degeneration is unclear.
Methods:
Following treatment with the alkylating agent methyl methane sulfonate (MMS), the C3 mRNA and protein level was measured, DNA damage and photoreceptor cell death were assessed in both wild-type (WT) C57BL/6J and C3 knockout (KO) mice.
Results:
We determined that complement pathway is activated following MMS treatment, and C3 knockout (KO) increased the rate of photoreceptor cell survival and preserved visual function. The mRNA levels of nuclear erythroid-related factor 2 (Nrf2) and related genes were higher after MMS application in C3 KO mice.
Conclusion:
In summary, our study found that C3 KO promotes photoreceptor cell survival and activates the Nrf2 signaling pathway in the context of alkylation-induced retinal degeneration.
