Autoimmunity in retinal degeneration: Autoimmune retinopathy and age-related macular degeneration

2009 ◽  
Vol 33 (3-4) ◽  
pp. 247-254 ◽  
Author(s):  
Kei Morohoshi ◽  
Anne M. Goodwin ◽  
Masaharu Ohbayashi ◽  
Santa Jeremy Ono
Keyword(s):  
Macular Degeneration ◽  
Retinal Degeneration ◽  
Age Related Macular Degeneration ◽  
Autoimmune Retinopathy ◽  
Age Related

scholarly journals Potential Sources and Roles of Adaptive Immunity in Age-Related Macular Degeneration: Shall We Rename AMD into Autoimmune Macular Disease?

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Serge Camelo
Keyword(s):  
T Cells ◽  
Macular Degeneration ◽  
Retinal Degeneration ◽  
Adaptive Immunity ◽  
Choroidal Neovascularization ◽  
Vision Loss ◽  
Retinal Pigment ◽  
Age Related Macular Degeneration ◽  
Age Related ◽  
Pathologic Features

Age-related macular degeneration (AMD) is the leading cause of vision loss in the elderly throughout the industrialized world. Its most prominent pathologic features are lesions involving the retinal pigment epithelium (RPE) the Bruch’s membrane, the degeneration of photoreceptors, and, in the most aggressive cases, choroidal neovascularization. Genetic associations between the risk of developing AMD and polymorphism within components of the complement system, as well as chemokine receptors expressed on microglial cells and macrophages, have linked retinal degeneration and choroidal neovascularization to innate immunity (inflammation). In addition to inflammation, players of the adaptive immunity including cytokines, chemokines, antibodies, and T cells have been detected in animal models of AMD and in patients suffering from this pathology. These observations suggest that adaptive immunity might play a role in different processes associated with AMD such as RPE atrophy, neovascularization, and retinal degeneration. To this date however, the exact roles (if any) of autoantibodies and T cells in AMD remain unknown. In this review we discuss the potential effects of adaptive immune responses in AMD pathogenesis.

scholarly journals Functional microRNA targetome undergoes degeneration-induced shift in the retina

2020 ◽  
Author(s):  
Joshua A. Chu-Tan ◽  
Zhi-Ping Feng ◽  
Yvette Wooff ◽  
Adrian V. Cioanca ◽  
Ulrike Schumann ◽  
...  
Keyword(s):  
Mouse Model ◽  
Neurodegenerative Diseases ◽  
Macular Degeneration ◽  
Retinal Degeneration ◽  
Significant Role ◽  
Age Related Macular Degeneration ◽  
Retinal Damage ◽  
Regulatory Activity ◽  
Age Related ◽  
Insight Into

SummaryMicroRNA (miRNA) play a significant role in the pathogenesis of complex neurodegenerative diseases, including age-related macular degeneration, acting as post-transcriptional gene suppressors through their association with argonaute (AGO) protein family members. However, to understand their role in disease, investigation into the regulatory nature of miRNA with their targets is required. To identify the active-miRnome-targetome interactions in the degenerating retina, AGO2 HITS-CLIP was performed using a mouse model of retinal degeneration. Analysis revealed a similar miRnome between healthy and damaged retinas, however, a shift in the active targetome was observed. This shift was also demonstrated by a change in the seed binding regions of miR-124-3p, the most abundant retinal miRNA loaded in AGO2. Following damage, AGO2 was localised to the inner retinal layers indicating a locational miRNA response to retinal damage. This study provides important insight into the alteration of miRNA regulatory activity that occurs as a response to retinal degeneration.

scholarly journals Age-related macular degeneration-like phenotypic features develop at the early ages of Cxcr5/Nrf2 double knockout mice: An accelerated AMD model

2019 ◽  
Author(s):  
Hu Huang ◽  
Anton Lennikov
Keyword(s):  
Protein Expression ◽  
Macular Degeneration ◽  
Retinal Degeneration ◽  
Cell Apoptosis ◽  
Age Related Macular Degeneration ◽  
Double Knockout ◽  
Western Blots ◽  
Age Related ◽  
Associated Proteins ◽  
Phenotypic Features

AbstractAge-related macular degeneration (AMD) is a leading cause of blindness for older adults. The aim of this study is to develop an accelerated mouse model of AMD and characterize its phenotypic features. Cxcr5 knockout (KO) mice and Nrf2 KO mice were bred to create Cxcr5/Nrf2 double knockout (DKO) mice. AMD-like features in Cxcr5/Nrf2 DKO mice were compared with those in CXCR5 KO mice and C57BL6 wild-type (WT) controls. The assessment included fundus and optical coherence tomography (OCT) imaging, periodic acid-Schiff (PAS) and immunofluorescence staining of retinal pigment epithelium (RPE)–choroid flat mounts and sections. Stained samples were imaged with fluorescent microscopy, and Western blots were used to monitor protein expression changes. The staining of cleaved caspase-3, peanut agglutinin (PNA) lectin, and MAP2 was performed to assess the presence of retinal degeneration and cell apoptosis. Quantification with statistical analysis was performed with Graphpad software. The 2- 4-, and 6-month-old DKO mice exhibited increased hypopigmented spots on fundus and sub-RPE abnormalities on OCT as compared to the Cxcr5 KO mice, and C57BL6 WT controls. Aberrant RPE/sub-RPE depositions and increased Bruch’s membrane (BM) thickness were demonstrated by PAS-stained sections. The DKO mice had strong autofluorescence (A2E) and increased RPE/sub-RPE depositions of IgG and AMD-associated proteins (β amyloid, Apolipoprotein E, complement 5b-9, and αB-crystallin). The protein expression of AMD-associated proteins and Transmembrane Protein 119 (TMEM119) microglia marker were upregulated at the RPE/BM/choroid complex of DKO mice. The adult DKO mice underwent accelerated retinal degeneration and cell apoptosis compared to the KO and the WT mice. Together, the data suggest that the Cxcr5/Nrf2 DKO mice develop significant AMD-like characteristics at an early age and may serve as an accelerated AMD model.Sumary StatementA new animal model is developed to mimic early AMD characteristics in adult mice

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