ArticlePloS one2014
Synthesis and propagation of complement C3 by microglia/monocytes in the aging retina.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 57 citations in OpenAlex.
- Role of P2X7R in Retinal Diseases: A Review.Immunity, inflammation and disease · 2025Review
- Myeloid lineage C3 induces reactive gliosis and neuronal stress during CNS inflammation.Nature communications · 2025Article
- Moss-derived human complement factor H modulates retinal immune response and attenuates retinal degeneration.Journal of neuroinflammation · 2025Article
- Unraveling the immune response in optic nerve injury: implications for retinal ganglion cell protection.Frontiers in immunology · 2025Review
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- Vitreous humor proteome: unraveling the molecular mechanisms underlying proliferative and neovascular vitreoretinal diseases.Cellular and molecular life sciences : CMLS · 2022Review
- Review
- Fecal microbiota transfer between young and aged mice reverses hallmarks of the aging gut, eye, and brain.Microbiome · 2022Article
- Complement factor H deficiency combined with smoking promotes retinal degeneration in a novel mouse model.Experimental biology and medicine (Maywood, N.J.) · 2022Article
- Molecular Mechanisms Related to Oxidative Stress in Retinitis Pigmentosa.Antioxidants (Basel, Switzerland) · 2021Review
- Inhibition of microRNA-155 Protects Retinal Function Through Attenuation of Inflammation in Retinal Degeneration.Molecular neurobiology · 2021Article
- Cytokine and Complement Response in the Glaucomatous βB1-CTGF Mouse Model.Frontiers in cellular neuroscience · 2021Article
- Innate Immunity in Age-Related Macular Degeneration.Advances in experimental medicine and biology · 2021Article
- Caspase-1-dependent inflammasomes mediate photoreceptor cell death in photo-oxidative damage-induced retinal degeneration.Scientific reports · 2020Article
- Control of Complement Activation by the Long Pentraxin PTX3: Implications in Age-Related Macular Degeneration.Frontiers in pharmacology · 2020Article
- Ablation of C3 modulates macrophage reactivity in the outer retina during photo-oxidative damage.Molecular vision · 2020Article
- A Systematic Investigation on Complement Pathway Activation in Diabetic Retinopathy.Frontiers in immunology · 2020Article
- C3- and CR3-dependent microglial clearance protects photoreceptors in retinitis pigmentosa.The Journal of experimental medicine · 2019Article
- Subretinal macrophages produce classical complement activator C1q leading to the progression of focal retinal degeneration.Molecular neurodegeneration · 2018Article
- MicroRNA-124 Dysregulation is Associated With Retinal Inflammation and Photoreceptor Death in the Degenerating Retina.Investigative ophthalmology & visual science · 2018Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionComplement activation is thought to contribute to the pathogenesis of age-related macular degeneration (AMD), which may be mediated in part by para-inflammatory processes. We aimed to investigate the expression and localization of C3, a crucial component of the complement system, in the retina during the course of aging.
methodsSD rats were born and reared in low-light conditions, and euthanized at post-natal (P) days 100, 450, or 750. Expression of C3, IBA1, and Ccl- and Cxcl- chemokines was assessed by qPCR, and in situ hybridization. Thickness of the ONL was assessed in retinal sections as a measure of photoreceptor loss, and counts were made of C3-expressing monocytes.
resultsC3 expression increased significantly at P750, and correlated with thinning of the ONL, at P750, and up-regulation of GFAP. In situ hybridization showed that C3 was expressed by microglia/monocytes, mainly from within the retinal vasculature, and occasionally the ONL. The number of C3-expressing microglia increased significantly by P750, and coincided spatiotemporally with thinning of the ONL, and up-regulation of Ccl- and Cxcl- chemokines.
conclusionsOur data suggest that recruited microglia/monocytes contribute to activation of complement in the aging retina, through local expression of C3 mRNA. C3 expression coincides with age-related thinning of the ONL at P750, although it is unclear whether the C3-expressing monocytes are a cause or consequence. These findings provide evidence of activation of complement during natural aging, and may have relevance to cellular events underling the pathogenesis of age-related retinal diseases.
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