ArticleInvestigative ophthalmology & visual science2012
Lack of immunoglobulins does not prevent C1q binding to RGC and does not alter the progression of experimental glaucoma.
Article in Investigative ophthalmology & visual science, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 25 citations in OpenAlex.
- C-reactive protein dissociation drives choroidal neovascularization in age-related macular degeneration.Scientific reports · 2025Article
- Visible light optical coherence tomography for assessing retinal structure and function in diseased mouse models.Biomedical optics express · 2025Article
- Review
- The Role of Complement Dysregulation in Glaucoma.International journal of molecular sciences · 2024Review
- Retinal Ganglion Cell Axon Regeneration Requires Complement and Myeloid Cell Activity within the Optic Nerve.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Early Functional Impairment in Experimental Glaucoma Is Accompanied by Disruption of the GABAergic System and Inceptive Neuroinflammation.International journal of molecular sciences · 2021Article
- T Cell-Mediated Autoimmunity in Glaucoma Neurodegeneration.Frontiers in immunology · 2021Review
- Complement-Mediated Microglial Phagocytosis and Pathological Changes in the Development and Degeneration of the Visual System.Frontiers in immunology · 2020Review
- The Association of Oxidative Stress Status with Open-Angle Glaucoma and Exfoliation Glaucoma: A Systematic Review and Meta-Analysis.Journal of ophthalmology · 2019Review
- Oral Delivery of a Synthetic Sterol Reduces Axonopathy and Inflammation in a Rodent Model of Glaucoma.Frontiers in neuroscience · 2017Article
- Exercise reverses age-related vulnerability of the retina to injury by preventing complement-mediated synapse elimination via a BDNF-dependent pathway.Aging cell · 2016Article
- Transplantation of iPSC-derived TM cells rescues glaucoma phenotypes in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Cryopreserved Mesenchymal Stromal Cells Maintain Potency in a Retinal Ischemia/Reperfusion Injury Model: Toward an off-the-shelf Therapy.Scientific reports · 2016Article
- Immune response after intermittent minimally invasive intraocular pressure elevations in an experimental animal model of glaucoma.Journal of neuroinflammation · 2016Article
- Adoptive transfer of immune cells from glaucomatous mice provokes retinal ganglion cell loss in recipients.Acta neuropathologica communications · 2015Article
- Clusterin and complement activation in exfoliation glaucoma.Investigative ophthalmology & visual science · 2014Article
- Apoptotic retinal ganglion cell death in an autoimmune glaucoma model is accompanied by antibody depositions.Journal of molecular neuroscience : MN · 2014Article
- Immune regulation toward immunomodulation for neuroprotection in glaucoma.Current opinion in pharmacology · 2013Review
- Immunoproteomic analysis of potential serum biomarker candidates in human glaucoma.Investigative ophthalmology & visual science · 2012Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
purposeThe degeneration of retinal ganglion cells (RGC) in the glaucomatous retina is accompanied by activation of the classical complement cascade. The purpose of this study was to evaluate whether complement component C1q binding and activation of the complement cascade in the glaucomatous retina requires the presence of immunoglobulins.
methodsExperimental glaucoma was induced in normal mice and those carrying a targeted deletion of the RAG1 gene. Binding of C1q to RGC and accumulation of C3 and C5b-9 was investigated using immunohistochemical and proteomic approaches. Damage to the optic nerve and RGC was determined and compared between the two strains. Complement activation and accumulation were also evaluated in vitro using dissociated retinal cell cultures.
resultsC1q was detected in the RGC layer in both RAG1(-/-) and control mice with elevated IOP, but not in mice with normal IOP. Proteomic analysis of retinal membrane fractions indicated that C1q and C3 are membrane bound to a similar degree in RAG1(-/-) and control mice with elevated IOP. The absence of Ig does not affect the rate of axonal damage or RGC loss. Furthermore, cultured RGC maintained in serum-free media are also C1q and C3 immunoreactive, demonstrating that Ig is not required for C1q binding to damaged RGC.
conclusionsOur data demonstrate that lack of immunoglobulins and mature T/B cells does not influence the progression of glaucoma. Furthermore, immunoglobulins do not appear to be required for C1q binding and complement cascade activation on damaged RGC. These findings suggest that C1q recognizes an alternative binding partner expressed by stressed RGC.
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