Systemic expression of Alu RNA in patients with geographic atrophy secondary to age-related macular degeneration.

Geographic atrophy (GA) secondary to age-related macular degeneration (AMD) is characterized by irreversible loss of macular retinal tissue and retinal pigment epithelium (RPE) cells. Several studies have revealed that accumulation of Alu RNA in RPE cell causes RPE cell degeneration in AMD. In the p...

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Main Authors: Hiroyuki Yoshida, Tokiyoshi Matsushita, Erika Kimura, Yukie Fujita, Robert Keany, Toshihiro Ikeda, Masanao Toshimori, Takahiro Imanaka, Masatsugu Nakamura
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2019-01-01
Series:PLoS ONE
Online Access:https://doi.org/10.1371/journal.pone.0220887
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spelling doaj-e71ee32534944c7dbe7bc58e3a699a742021-03-03T21:15:52ZengPublic Library of Science (PLoS)PLoS ONE1932-62032019-01-01148e022088710.1371/journal.pone.0220887Systemic expression of Alu RNA in patients with geographic atrophy secondary to age-related macular degeneration.Hiroyuki YoshidaTokiyoshi MatsushitaErika KimuraYukie FujitaRobert KeanyToshihiro IkedaMasanao ToshimoriTakahiro ImanakaMasatsugu NakamuraGeographic atrophy (GA) secondary to age-related macular degeneration (AMD) is characterized by irreversible loss of macular retinal tissue and retinal pigment epithelium (RPE) cells. Several studies have revealed that accumulation of Alu RNA in RPE cell causes RPE cell degeneration in AMD. In the present study, systemic Alu RNA expression levels were determined in 33 subjects with GA and 40 control subjects using a proprietary Alu RNA quantification method. It was observed that the expression level of Alu RNA was not significantly different between GA and Control groups (median = 21.3 in both GA and Control groups, P = 0.251). In addition, the systemic level of Alu RNA was not associated with subject characteristics, such as GA lesion size and SNP profiles of complement factors associated with increased risk of AMD. In conclusion, the usability of systemic Alu RNA expression level as a biomarker of GA secondary to AMD could not be established in this study.https://doi.org/10.1371/journal.pone.0220887
collection DOAJ
language English
format Article
sources DOAJ
author Hiroyuki Yoshida
Tokiyoshi Matsushita
Erika Kimura
Yukie Fujita
Robert Keany
Toshihiro Ikeda
Masanao Toshimori
Takahiro Imanaka
Masatsugu Nakamura
spellingShingle Hiroyuki Yoshida
Tokiyoshi Matsushita
Erika Kimura
Yukie Fujita
Robert Keany
Toshihiro Ikeda
Masanao Toshimori
Takahiro Imanaka
Masatsugu Nakamura
Systemic expression of Alu RNA in patients with geographic atrophy secondary to age-related macular degeneration.
PLoS ONE
author_facet Hiroyuki Yoshida
Tokiyoshi Matsushita
Erika Kimura
Yukie Fujita
Robert Keany
Toshihiro Ikeda
Masanao Toshimori
Takahiro Imanaka
Masatsugu Nakamura
author_sort Hiroyuki Yoshida
title Systemic expression of Alu RNA in patients with geographic atrophy secondary to age-related macular degeneration.
title_short Systemic expression of Alu RNA in patients with geographic atrophy secondary to age-related macular degeneration.
title_full Systemic expression of Alu RNA in patients with geographic atrophy secondary to age-related macular degeneration.
title_fullStr Systemic expression of Alu RNA in patients with geographic atrophy secondary to age-related macular degeneration.
title_full_unstemmed Systemic expression of Alu RNA in patients with geographic atrophy secondary to age-related macular degeneration.
title_sort systemic expression of alu rna in patients with geographic atrophy secondary to age-related macular degeneration.
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2019-01-01
description Geographic atrophy (GA) secondary to age-related macular degeneration (AMD) is characterized by irreversible loss of macular retinal tissue and retinal pigment epithelium (RPE) cells. Several studies have revealed that accumulation of Alu RNA in RPE cell causes RPE cell degeneration in AMD. In the present study, systemic Alu RNA expression levels were determined in 33 subjects with GA and 40 control subjects using a proprietary Alu RNA quantification method. It was observed that the expression level of Alu RNA was not significantly different between GA and Control groups (median = 21.3 in both GA and Control groups, P = 0.251). In addition, the systemic level of Alu RNA was not associated with subject characteristics, such as GA lesion size and SNP profiles of complement factors associated with increased risk of AMD. In conclusion, the usability of systemic Alu RNA expression level as a biomarker of GA secondary to AMD could not be established in this study.
url https://doi.org/10.1371/journal.pone.0220887
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