The DOI matches its Crossref record; 37 of the 37 references it cites were found in a registry or an index.
Complement Activation via Alternative Pathway Is Critical in the Development of Laser-Induced Choroidal Neovascularization: Role of Factor B and Factor H
Abstract
The objective of this study was to explore the role of classical, lectin, and alternative pathways of complement activation in laser-induced choroidal neovascularization (CNV). The classical and alternative pathways were blocked in C57BL/6 mice by small interfering RNAs (siRNA) directed against C1q and factor B, respectively. C4−/− mice developed CNV similar to their wild-type controls and inhibition of C1q by siRNA had no effect on the development of CNV. In contrast, CNV was significantly inhibited (p < 0.001) in C5−/− mice and C57BL/6 mice treated with factor B siRNA. Inhibition of the alternative pathway by factor B siRNA resulted in decreased levels of membrane attack complex and angiogenic factors–vascular endothelial growth factor and TGF-β2. Furthermore, factor B was up-regulated in complement sufficient C57BL/6 mice at day 1 postlaser and remained elevated at day 7. Significantly reduced levels of factor H were observed at day 3 in these animals. In conclusion, our results demonstrate that activation of the factor B-dependent alternative pathway, but not the classical or lectin pathways, was essential for the development of CNV in mouse model of laser-induced CNV. Thus, specific blockade of the alternative pathway may represent a therapeutically relevant strategy for the inhibition of CNV.
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“Several experiments using mouse models of laser-induced CNV have demonstrated that all complement pathways, particularly the alternative and terminal pathways, play a significant role in angiogenesis [150,152,153,154,155,156,157,158,159,160,161,162,163].”
From Bruch’s Membrane: A Key Consideration with Complement-Based Therapies for Age-Related Macular Degeneration (2023) · cites this paper as [154]
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Cited by
Sorted by citations
Vascular endothelial growth factor in eye disease
Penn, J. S., Madan, A., Caldwell, R. B., Bartoli, M., Caldwell, R. W., & Hartnett, M. E. (2008) · Progress in Retinal and Eye Research · doi:10.1016/j.preteyeres.2008.05.001 · Cited by 784
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Metadata
- Authors
- Bora, N. S., Kaliappan, S., Jha, P., Xu, Q., Sohn, J.-H., Dhaulakhandi, D. B., Kaplan, H. J., & Bora, P. S.
- Affiliations
- University of Arkansas for Medical Sciences (US)
- University of Louisville (US)
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2006-08-01
- Volume
- 177
- Issue
- 3
- Pages
- 1872-1878
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W1585939626
- Cited by
- 124
- References
- 37
- Citations by year
- 2025: 1 · 2024: 3 · 2023: 4 · 2022: 7 · 2021: 4 · 2020: 7 · 2019: 1 · 2018: 5 · 2017: 11 · 2016: 5 · 2015: 8 · 2014: 9 · 2013: 4 · 2012: 12
- FWCI
- 3.42
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Eye Institute (R01EY013335, R01EY014623, EY 014623, EY-13335)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Complement system in diseases
- Health Sciences › Medicine › Ophthalmology › Retinal Diseases and Treatments
- Health Sciences › Medicine › Ophthalmology › Ocular Diseases and Behçet’s Syndrome
- Keywords
- choroidal neovascularization, laser-induced CNV, alternative complement pathway, factor B, complement factor H, complement activation, C1q, C5, membrane attack complex, angiogenesis, vascular endothelial growth factor, TGF-beta2, siRNA knockdown
- MeSH terms
- Animals, Complement Pathway, Alternative, Complement C4, Complement C5, Injections, Intravenous, Lasers, Male, Mice, Inbred C57BL, Complement Factor B, Down-Regulation, Up-Regulation, Complement C1q, Complement Membrane Attack Complex, Transforming Growth Factor beta, Complement Factor H, Mice, Knockout, Choroidal Neovascularization, RNA, Small Interfering, Vascular Endothelial Growth Factor A, Mice, Transforming Growth Factor beta2
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