Abstract
This study explored the expression of several miRNAs reported to be deregulated in age-related macular degeneration (AMD). Total RNA was isolated from sera from patients with dry AMD (n = 12), wet AMD (n = 14), and controls (n = 10). Forty-two previously investigated miRNAs were selected based on published data and their role in AMD pathogenesis, such as angiogenic and inflammatory effects, and were co-analysed using a miRCURY LNA miRNA SYBR® Green PCR kit via quantitative real-time polymerase chain reaction (qRT-PCR) to validate their presence. Unsupervised hierarchical clustering indicated that AMD serum specimens have a different miRNA profile to healthy controls. We successfully validated the differentially regulated miRNAs in serum from AMD patients versus controls. Eight miRNAs (hsa-let-7a-5p, hsa-let-7d-5p, hsa-miR-23a-3p, hsa-miR-301a-3p, hsa-miR-361-5p, hsa-miR-27b-3p, hsa-miR-874-3p, hsa-miR-19b-1-5p) showed higher expression in the serum of dry AMD patients than wet AMD patients and compared with healthy controls. Increased quantities of certain miRNAs in the serum of AMD patients indicate that these miRNAs could potentially serve as diagnostic AMD biomarkers and might be used as future AMD treatment targets. The discovery of significant serum miRNA biomarkers in AMD patients would provide an easy screening tool for at-risk populations.
Highlights
Age-related macular degeneration (AMD) is the most common cause of blindness in people over 60 years of age [1,2,3]
Our study successfully profiled the differential quantities of miRNAs in serum from AMD patients compared with healthy controls in an Irish context
Of the candidate miRNAs selected for examination, 39 were significantly up-regulated in the serum of AMD patients compared with controls, validating their usefulness as potential biomarkers for AMD in Irish patients (Table 2, Figure 4)
Summary
Age-related macular degeneration (AMD) is the most common cause of blindness in people over 60 years of age [1,2,3]. Atrophic AMD is characterised in its early stages by dysfunction of the retinal pigment epithelium (RPE) along with the formation of drusen in Bruch’s membrane [4,5]. These changes result in atrophy and damage to the photoreceptor cells and RPE which in turn results in a slow, progressive, and irreversible loss of vision [4,5]. Neovascular AMD is another form of late-stage disease, where loss of vision is attributable to the formation of new vessels within and below the retina via choroidal neovascularisation [2,6,7] These new vessels are disorganised, friable and prone to haemorrhage, aberrant fibrovascular scarring and detachment, and RPE [1,2,5,7]. The progression of visual loss is markedly more rapid in neovascular AMD compared to atrophic AMD [2,6,8]
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