Molecular response of chorioretinal endothelial cells to complement injury: Implications for macular degeneration
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Age‐related macular degeneration ( AMD ) is a common, blinding disease of the elderly in which macular photoreceptor cells, retinal pigment epithelium and choriocapillaris endothelial cells ultimately degenerate. Recent studies have found that degeneration of the choriocapillaris occurs early in this disease and that endothelial cell drop‐out is concomitant with increased deposition of the complement membrane attack complex ( MAC ) at the choroidal endothelium. However, the impact of MAC injury to choroidal endothelial cells is poorly understood. To model this event in vitro , and to study the downstream consequences of MAC injury, endothelial cells were exposed to complement from human serum, compared to heat‐inactivated serum, which lacks complement components. Cells exposed to complement components in human serum showed increased labelling with antibodies directed against the MAC , time‐ and dose‐dependent cell death, as assessed by lactate dehydrogenase assay and increased permeability. RNA ‐Seq analysis following complement injury revealed increased expression of genes associated with angiogenesis including matrix metalloproteinase ( MMP )‐3 and −9, and VEGF ‐A. The MAC ‐induced increase in MMP9 RNA expression was validated using C5 ‐depleted serum compared to C5 ‐reconstituted serum. Increased levels of MMP9 were also established, using western blot and zymography. These data suggest that, in addition to cell lysis, complement attack on choroidal endothelial cells promotes an angiogenic phenotype in surviving cells. Copyright © 2015 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
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MMP expression in choroidal endothelial cells has been found to increase with MAC-dependent complement activation, suggesting that complement may promote angiogenesis through multiple pathways.
“MMP expression in choroidal endothelial cells has also been found to increase with MAC-dependent complement activation [172], suggesting that complement may promote angiogenesis through multiple pathways.”
From Bruch’s Membrane: A Key Consideration with Complement-Based Therapies for Age-Related Macular Degeneration (2023) · cites this paper as [172]
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Ref-1 is overexpressed in neovascular eye disease and targetable with a novel inhibitor
Muniyandi, A., Hartman, G. D., Sishtla, K. L., Rai, R., Gomes, C., Day, K., Song, Y., Masters, A. R., Quinney, S. K., Qi, X., et al. (2025) · Angiogenesis · doi:10.1007/s10456-024-09966-0 · Cited by 9 · see citing works
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Imidazole Compounds for Protecting Choroidal Endothelial Cells from Complement Injury
Zeng, S., Wen, K., Workalemahu, G., Sohn, E. H., Wu, M., Chirco, K. R., Flamme‐Wiese, M. J., Liu, X., Stone, E. M., Tucker, B. A., et al. (2018) · Scientific Reports · doi:10.1038/s41598-018-31846-z · Cited by 9 · see citing works
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A Revised Hemodynamic Theory of Age-Related
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Self-citationExploring Endotoxemia in Age-Related Macular Degeneration, Glaucoma, and Diabetic Retinopathy
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- Authors
- Zeng, S., Whitmore, S. S., Sohn, E. H., Riker, M. J., Wiley, L. A., Scheetz, T. E., Stone, E. M., Tucker, B. A., & Mullins, R. F.
- Affiliations
- University of Iowa (US)
- Corresponding author
- Mullins, Robert F
- ORCID
- Venue
- The Journal of Pathology
- Publisher
- Wiley
- Published
- 2015-12-24
- Volume
- 238
- Issue
- 3
- Pages
- 446-456
- ISSN
- 0022-3417 (ISSN-L)
- 1096-9896
- PMC
- PMC4900182
- OpenAlex
- W2171447320
- Cited by
- 56
- References
- 43
- Citations by year
- 2026: 3 · 2025: 3 · 2024: 3 · 2023: 3 · 2022: 6 · 2021: 11 · 2020: 3 · 2019: 6 · 2018: 8 · 2017: 5 · 2016: 5
- FWCI
- 5.77
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Journal of Pathology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (EY‐024605, EY‐023187, 1‐DP2‐OD007483‐01)
- 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
- age-related macular degeneration, membrane attack complex, endothelial cell death, endothelial permeability, angiogenesis, MMP-9, matrix metalloproteinase-3, VEGF-A, choroidal degeneration
- MeSH terms
- Aged, Aged, 80 and over, Antibodies, Cells, Cultured, Choroid, Complement System Proteins, Complement Activation, Dose-Response Relationship, Immunologic, Female, Humans, Macular Degeneration, Male, Up-Regulation, Complement Membrane Attack Complex, Cell Death, Matrix Metalloproteinase 3, Matrix Metalloproteinase 9, Vascular Endothelial Growth Factor A, Endothelial Cells
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