ArticleScientific reports2015
Choroidal neovascularization is inhibited via an intraocular decrease of inflammatory cells in mice lacking complement component C3.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- CircAFF3 modulation of p53-ID2 signaling in the retinal pigment epithelium links inflammation with cell death in dry age-related macular degeneration.Frontiers in cell and developmental biology · 2026Article
- Cathepsin S Knockdown Suppresses Endothelial Inflammation, Angiogenesis, and Complement Protein Activity under Hyperglycemic Conditions In Vitro by Inhibiting NF-κB Signaling.International journal of molecular sciences · 2023Article
- C3-dependent effector functions of complement.Immunological reviews · 2023Review
- Article
- Evaluating a Causal Relationship between Complement Factor I Protein Level and Advanced Age-Related Macular Degeneration Using Mendelian Randomization.Ophthalmology science · 2022Article
- Cochlear Immune Response in Presbyacusis: a Focus on Dysregulation of Macrophage Activity.Journal of the Association for Research in Otolaryngology : JARO · 2022Review
- Incomplete response to Anti-VEGF therapy in neovascular AMD: Exploring disease mechanisms and therapeutic opportunities.Progress in retinal and eye research · 2021Review
- Immunological Aspects of Age-Related Macular Degeneration.Advances in experimental medicine and biology · 2021Article
- TLR4-dependent shaping of the wound site by MSCs accelerates wound healing.EMBO reports · 2020Article
- The role of lymphocytes and phagocytes in age-related macular degeneration (AMD).Cellular and molecular life sciences : CMLS · 2020Review
- Asian age-related macular degeneration: from basic science research perspective.Eye (London, England) · 2019Review
- New Therapies of Neovascular AMD-Beyond Anti-VEGFs.Vision (Basel, Switzerland) · 2018Review
- Classical and alternative complement activation on photoreceptor outer segments drives monocyte-dependent retinal atrophy.Scientific reports · 2018Article
- Suppression of aberrant choroidal neovascularization through activation of the aryl hydrocarbon receptor.Biochimica et biophysica acta. Molecular basis of disease · 2018Article
- Toll-like receptor-9 is involved in the development of B cell stimulating factor-induced systemic lupus erythematosus.Experimental and therapeutic medicine · 2018Article
- Idiopathic Choroidal Neovascularization: Intraocular Inflammatory Cytokines and the Effect of Intravitreal Ranibizumab Treatment.Scientific reports · 2016Article
- C3a Increases VEGF and Decreases PEDF mRNA Levels in Human Retinal Pigment Epithelial Cells.BioMed research international · 2016Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In early age-related macular degeneration (AMD), complement component C3 can be observed in drusen, which is the accumulation of material beneath the retinal pigment epithelium. The complement pathways, via the activation of C3, can upregulate the expression of cytokines and their receptors and the recruitment of inflammatory leukocytes, both of which play an important role in the development of choroidal neovascularization (CNV) in exudative AMD. Laser-induced CNV lesions were found to be significantly smaller in C3(-/-) mice than in wild-type mice. By using flow cytometry, we demonstrated that the proportions of intraocular granulocytes, CD11b(+)F4/80(+)Ly6C(hi) and CD11b(+)F4/80(+)Ly6C(lo) cells, were lower in C3(-/-) mice than in wild-type mice as early as day 1 after laser injury, and the proportions of granulocytes and three macrophage/monocyte subsets were significantly lower on day 3. In contrast, C3(-/-) mice had more granulocytes and CD11b(+)F4/80(+)Ly6C(hi) cells in peripheral blood than wild-type mice after injury. Further, the expression levels of Vegfa164 were upregulated in intraocular Ly6C(hi) macrophages/monocytes of C3(-/-) mice, but not as much as in wild-type mice. Collectively, our data demonstrate that despite a more pronounced induction of systemic inflammation, inhibition of complement factor C3 suppresses CNV by decreasing the recruitment of inflammatory cells to the lesion.
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