Treatment with interleukin‐33 is non‐toxic and protects retinal pigment epithelium in an ageing model of outer retinal degeneration

Autor: Jian Liu, Andrew D. Dick, Stephen E. Moss, Sofia Theodoropoulou, Alison J. Clare, Christopher R. Neal, Lindsay B. Nicholson, David A. Copland
Rok vydání: 2020
Předmět:
0301 basic medicine
Retinal degeneration
Aging
Pathology
medicine.medical_specialty
genetic structures
Short Communication
Short Communications
retinal pigment epithelium
IL‐33
Neovascularization
Macular Degeneration
Mice
03 medical and health sciences
chemistry.chemical_compound
0302 clinical medicine
Atrophy
medicine
Animals
Humans
Mice
Knockout
Retinal pigment epithelium
business.industry
Retinal Degeneration
age‐related macular degeneration
complement factor H
Retinal
Cell Biology
Macular degeneration
Interleukin-33
medicine.disease
Immunohistochemistry
eye diseases
Disease Models
Animal
Treatment Outcome
030104 developmental biology
Choroidal neovascularization
medicine.anatomical_structure
chemistry
030220 oncology & carcinogenesis
Factor H
Molecular Medicine
sense organs
medicine.symptom
business
Zdroj: Journal of Cellular and Molecular Medicine
Clare, A J, Copland, D A, Nicholson, L B, Liu, J, Neal, C R, Moss, S, Dick, A D & Theodoropoulou, S 2020, ' Treatment with interleukin-33 is non-toxic and protects retinal pigment epithelium in an ageing model of outer retinal degeneration ', Journal of Cellular and Molecular Medicine . https://doi.org/10.1111/jcmm.16000
ISSN: 1582-4934
1582-1838
DOI: 10.1111/jcmm.16000
Popis: The leading cause of central vision loss, age‐related macular degeneration (AMD), is a degenerative disorder characterized by atrophy of retinal pigment epithelium (RPE) and photoreceptors. For 15% of cases, neovascularization occurs, leading to acute vision loss if left untreated. For the remaining patients, there are currently no treatment options and preventing progressive RPE atrophy remains the main therapeutic goal. Previously, we have shown treatment with interleukin‐33 can reduce choroidal neovascularization and attenuate tissue remodelling. Here, we investigate IL‐33 delivery in aged, high‐fat diet (HFD) fed mice on a wildtype and complement factor H heterozygous knockout background. We characterize the non‐toxic effect following intravitreal injection of IL‐33 and further demonstrate protective effects against RPE cell death with evidence of maintaining metabolic retinal homeostasis of Cfh+/−~HFD mice. Our results further support the potential utility of IL‐33 to prevent AMD progression.
Databáze: OpenAIRE
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