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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.
Eye and Vision (London, England)
|June 8, 2022
Summary
Complement C3 (C3) knockout mice show improved photoreceptor cell survival and preserved vision after DNA-alkylating agent exposure. This suggests C3 plays a key role in alkylation-induced retinal degeneration.
Area of Science:
- Ophthalmology
- Immunology
- Toxicology
Background:
- Anticancer drugs with DNA-alkylating agents can induce retinal inflammation via toxic intermediates.
- Complement C3 (C3) is crucial in complement activation, and its dysregulation is linked to retinal diseases.
- The role of C3 in alkylation-induced retinal degeneration remains largely unknown.
Purpose of the Study:
- To investigate the role of Complement C3 (C3) in DNA-alkylating agent-induced retinal degeneration.
- To determine if C3 knockout impacts photoreceptor cell survival and visual function following exposure to methyl methane sulfonate (MMS).
Main Methods:
- Mice were treated with methyl methane sulfonate (MMS), a DNA-alkylating agent.
- C3 mRNA and protein levels were measured.
- DNA damage and photoreceptor cell death were assessed in wild-type and C3 knockout mice.
Main Results:
- MMS treatment activated the complement pathway.
- C3 knockout significantly increased photoreceptor cell survival and preserved visual function.
- Nuclear erythroid-related factor 2 (Nrf2) pathway activation was observed in C3 knockout mice post-MMS treatment.
Conclusions:
- Complement C3 knockout promotes photoreceptor cell survival in alkylation-induced retinal degeneration.
- C3 knockout activates the Nrf2 signaling pathway, potentially conferring neuroprotection.
