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Cited by 249Retinal Diseases and TreatmentsComplement system in diseasesOcular Diseases and Behçet’s Syndrome

The DOI matches its Crossref record; 48 of the 48 references it cites were found in a registry or an index.

Role of Complement and Complement Membrane Attack Complex in Laser-Induced Choroidal Neovascularization

Bora, Puran S, Sohn, Jeong-Hyeon, Cruz, Jose M C, Jha, Purushottam, Nishihori, Hiroki, Wang, Yali, Kaliappan, Sankaranarayanan, Kaplan, Henry J, Bora, Nalini S·2005·The Journal of Immunology
DOI 10.4049/jimmunol.174.1.491
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Abstract

Choroidal neovascularization (CNV), or choroidal angiogenesis, is the hallmark of age-related macular degeneration and a leading cause of visual loss after age 55. The pathogenesis of new choroidal vessel formation is poorly understood. Although inflammation has been implicated in the development of CNV, the role of complement in CNV has not been explored experimentally. A reliable way to produce CNV in animals is to rupture Bruch’s membrane with laser photocoagulation. A murine model of laser-induced CNV in C57BL/6 mice revealed the deposition of C3 and membrane attack complex (MAC) in the neovascular complex. CNV was inhibited by complement depletion using cobra venom factor and did not develop in C3−/− mice. Anti-murine C6 Abs in C57BL/6 mice inhibited MAC formation and also resulted in the inhibition of CNV. Vascular endothelial growth factor, TGF-β2, and β-fibroblast growth factor were elevated in C57BL/6 mice after laser-induced CNV; complement depletion resulted in a marked reduction in the level of these angiogenic factors. Thus, activation of complement, specifically the formation of MAC, is essential for the development of laser- induced choroidal angiogenesis in mice. It is possible that a similar mechanism may be involved in the pathophysiology of other angiogenesis essential diseases.

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Metadata

Authors
Bora, P. S., Sohn, J.-H., Cruz, J. M. C., Jha, P., Nishihori, H., Wang, Y., Kaliappan, S., Kaplan, H. J., & Bora, N. S.
Affiliations
University of Louisville (US)
ORCID
Venue
The Journal of Immunology
Publisher
Oxford University Press (OUP)
Published
2005-01-01
Volume
174
Issue
1
Pages
491-497
ISSN
  • 0022-1767 (ISSN-L)
  • 1550-6606
DOI
10.4049/jimmunol.174.1.491
OpenAlex
W1901360874
Cited by
249
References
48
Citations by year
2026: 3 · 2025: 4 · 2024: 10 · 2023: 9 · 2022: 6 · 2021: 11 · 2020: 13 · 2019: 6 · 2018: 7 · 2017: 11 · 2016: 6 · 2015: 13 · 2014: 15 · 2013: 8 · 2012: 15
FWCI
18.34
Type
journal article
Language
en
Open access
closed
Licence
academic.oup.com/pages/standard-publication-reuse-rights (vor)
Locations
  • The Journal of Immunology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (7r01ey009730-07)
  • National Eye Institute (R01 EY009730-07, R01EY013335, R01EY014623, EY 014623, EY-13335)
Topics
  • Health Sciences › Medicine › Ophthalmology › Retinal Diseases and Treatments
  • Life Sciences › Immunology and Microbiology › Immunology › Complement system in diseases
  • Health Sciences › Medicine › Ophthalmology › Ocular Diseases and Behçet’s Syndrome
Keywords
choroidal neovascularization, complement system, membrane attack complex, choroidal angiogenesis, age-related macular degeneration, laser photocoagulation, Bruch's membrane rupture, complement C3, complement depletion, cobra venom factor, vascular endothelial growth factor, TGF-beta2, basic fibroblast growth factor, angiogenic factors, mouse model
MeSH terms
Animals, Choroid, Complement Activation, Complement C3, Disease Models, Animal, Enzyme-Linked Immunosorbent Assay, Fibroblast Growth Factors, Immunohistochemistry, Lasers, Male, Complement Membrane Attack Complex, Transforming Growth Factor beta, Microscopy, Confocal, Reverse Transcriptase Polymerase Chain Reaction, Choroidal Neovascularization, Vascular Endothelial Growth Factor A, Mice, Transforming Growth Factor beta2

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