Molecular clustering identifies complement and endothelin induction as early events in a mouse model of glaucoma
Open accessAbstract
Glaucoma is one of the most common neurodegenerative diseases. Despite this, the earliest stages of this complex disease are still unclear. This study was specifically designed to identify early stages of glaucoma in DBA/2J mice. To do this, we used genome-wide expression profiling of optic nerve head and retina and a series of computational methods. Eyes with no detectable glaucoma by conventional assays were grouped into molecularly defined stages of disease using unbiased hierarchical clustering. These stages represent a temporally ordered sequence of glaucoma states. We then determined networks and biological processes that were altered at these early stages. Early-stage expression changes included upregulation of both the complement cascade and the endothelin system, and so we tested the therapeutic value of separately inhibiting them. Mice with a mutation in complement component 1a (C1qa) were protected from glaucoma. Similarly, inhibition of the endothelin system with bosentan, an endothelin receptor antagonist, was strongly protective against glaucomatous damage. Since endothelin 2 is potently vasoconstrictive and was produced by microglia/macrophages, our data provide what we believe to be a novel link between these cell types and vascular dysfunction in glaucoma. Targeting early molecular events, such as complement and endothelin induction, may provide effective new treatments for human glaucoma.
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In a mouse model of glaucoma, C1q and C3 are highly upregulated and deposited on retinal synapses, and C1q deficiency or microglial inactivation with minocycline provides significant neuroprotection.
“Indeed, in a mouse model of glaucoma, a neurodegenerative disease associated with RGC loss and gliosis, C1q and C3 are highly upregulated and deposited on retinal synapses and C1q deficiency or microglial ‘inactivation’ with minocycline provide significant neuroprotection (Howell et al., 2011; Steele et al., 2006; Stevens et al., 2007).”
From Microglia Sculpt Postnatal Neural Circuits in an Activity and Complement-Dependent Manner (2012) · cites this paper as Howell et al., 2011
The research article (p. 6) reports early retinal upregulation of C1qa, C1qb and C1qc and says C1qa localizes to retinal synapses. Table 1 (p. 7) and Figure 8 (p. 11) show substantial protection in C1qa-deficient mice. Our copy does not establish C3 deposition on retinal synapses or neuroprotection from microglial inactivation with minocycline. (LLM, conf=0.89)
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Self-citation
- Authors
- Howell, G. R., Macalinao, D. G., Sousa, G. L., Walden, M., Soto, I., Kneeland, S. C., Barbay, J. M., King, B. L., Marchant, J. K., Hibbs, M., Stevens, B., Barres, B. A., Clark, A. F., Libby, R. T., & John, S. W. M.
- Affiliations
- Howard Hughes Medical Institute (US)
- Jackson Laboratory (US)
- Mount Desert Island Biological Laboratory (US)
- Tufts University (US)
- Harvard University (US)
- Stanford University (US)
- University of North Texas Health Science Center (US)
- University of Rochester (US)
- Corresponding author
- John, Simon W.M.
- ORCID
- Venue
- Journal of Clinical Investigation
- Published
- 2011-04-01
- Volume
- 121
- Issue
- 4
- Pages
- 1429-1444
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC3069778
- OpenAlex
- W1983740408
- Cited by
- 473
- References
- 77
- Citations by year
- 2026: 25 · 2025: 28 · 2024: 20 · 2023: 46 · 2022: 43 · 2021: 34 · 2020: 39 · 2019: 26 · 2018: 24 · 2017: 33 · 2016: 29 · 2015: 35 · 2014: 24 · 2013: 28 · 2012: 28
- FWCI
- 26.40
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- The Mouseion at the JAXlibrary (Jackson Laboratory) (submittedVersion)
- Funders
- Howard Hughes Medical Institute
- American Health Assistance Foundation
- Research to Prevent Blindness
- National Institutes of Health (NIH T32, EY011721)
- National Eye Institute (EY018606, R29EY011721, R01EY018606, R01EY011721, EY011721, F32EY014515)
- National Institute of Neurological Disorders and Stroke (T32 NS51112-05, T32NS051112)
- Topics
- Health Sciences › Medicine › Ophthalmology › Glaucoma and retinal disorders
- Health Sciences › Medicine › Ophthalmology › Retinal Diseases and Treatments
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Retinal Imaging and Analysis
- Keywords
- glaucoma, early-stage disease, complement system, endothelin system, endothelin receptor antagonism, bosentan, C1QA, optic nerve head, retina, microglia/macrophages, vascular dysfunction, disease progression, therapeutic target, DBA/2J mice
- MeSH terms
- Bosentan, Animals, Disease Models, Animal, Female, Glaucoma, Humans, Mice, Inbred DBA, Mice, Mutant Strains, Optic Nerve, Retina, Sulfonamides, Signal Transduction, Up-Regulation, Complement C1q, Cluster Analysis, Endothelin-2, Gene Expression Profiling, Mice, Endothelin Receptor Antagonists
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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