ArticleInvestigative ophthalmology & visual science2013
Age-dependent changes in FasL (CD95L) modulate macrophage function in a model of age-related macular degeneration.
Article in Investigative ophthalmology & visual science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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25 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.
- Markers of the ageing macrophage: a systematic review and meta-analysis.Frontiers in immunology · 2023Pooled it
- The role of IGF2BP2 in macrophage-mediated NLRP3 inflammasome activation in the pathogenesis of dry AMD.Biology direct · 2025Article
- Healthy and premature aging of monocytes and macrophages.Frontiers in immunology · 2025Review
- Role of macrophage in ocular neovascularization.Heliyon · 2024Review
- LXR/CD38 activation drives cholesterol-induced macrophage senescence and neurodegeneration via NADCell reports · 2024Article
- Fas Ligand enhances vessel maturation and inhibits vascular leakage associated with age-related macular degeneration.Research square · 2024Article
- Crosstalk Between Microglia and Müller Glia in the Age-Related Macular Degeneration: Role and Therapeutic Value of Neuroinflammation.Aging and disease · 2024Review
- Article
- CCR1 mediates Müller cell activation and photoreceptor cell death in macular and retinal degeneration.eLife · 2023Article
- Thymus antibody-secreting cells: once forgotten but not lost.Frontiers in immunology · 2023Article
- Cytokine Profiles and the Effect of Intravitreal Aflibercept Treatment on Experimental Choroidal Neovascularization.Ophthalmic research · 2022Article
- Incomplete response to Anti-VEGF therapy in neovascular AMD: Exploring disease mechanisms and therapeutic opportunities.Progress in retinal and eye research · 2021Review
- Immunological Aspects of Age-Related Macular Degeneration.Advances in experimental medicine and biology · 2021Article
- Article
- MicroRNA-155 Inhibits Polarization of Macrophages to M2-Type and Suppresses Choroidal Neovascularization.Inflammation · 2018Article
- Protective Effect of Met12, a Small Peptide Inhibitor of Fas, on the Retinal Pigment Epithelium and Photoreceptor After Sodium Iodate Injury.Investigative ophthalmology & visual science · 2017Article
- Inflammation and its role in age-related macular degeneration.Cellular and molecular life sciences : CMLS · 2016Review
- Bone marrow-derived cells in ocular neovascularization: contribution and mechanisms.Angiogenesis · 2016Review
- Defects in retinal pigment epithelial cell proteolysis and the pathology associated with age-related macular degeneration.Progress in retinal and eye research · 2016Review
- How Mouse Macrophages Sense What Is Going On.Frontiers in immunology · 2016Review
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5 authors.
Funding
Abstract
purposeWe examined the effect of aging on Fas ligand (FasL) function in a mouse model of choroidal neovascularization (CNV).
methodsYoung and aged mice were laser treated to induce CNV. Bone marrow chimeras were performed between young and aged mice. FasL protein expression was examined in the eye and soluble FasL (sFasL) was measured in the blood. Young and aged mice were treated with a matrix metalloprotease (MMP) inhibitor and systemic sFasL was neutralized by antibody treatment. Macrophages from young and aged mice were tested for sFasL-mediated cytokine production and migration.
resultsThe elevated CNV response observed with aging was dependent on bone marrow-derived cells. FasL expression in the eye was increased with age, but decreased following laser treatment. Aged mice had higher levels of sFasL in the blood compared to young mice. Systemic treatment with an MMP inhibitor decreased bloodborne sFasL, and reduced CNV in young and aged mice. Systemic neutralization of sFasL reduced CNV only in aged mice. sFasL increased cytokine production in aged macrophages and proangiogenic M2 macrophages. Aged M2 macrophages had elevated Fas (CD95) expression and displayed increased migration in response to sFasL compared to M1 macrophages derived from young animals.
conclusionsAge modulates FasL function where increased MMP cleavage leads to a loss of function in the eye. The released form of FasL (sFasL) preferentially induces the migration of proangiogenic M2 macrophages into the laser lesions and increases proangiogenic cytokines promoting CNV. FasL may be a viable target for therapeutic intervention in aged-related neovascular disease.
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