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Effect of Lecithin-Bound Iodine Treatment on Inherited Retinal Degeneration in Mice

PURPOSE: Although lecithin-bound iodine (LBI) has been administered orally for retinal diseases, a lack of clinical studies and obscure action mechanism of LBI hinder its large-scale prescription. LBI treatment suppresses chemokine (C-C motif) ligand 2 (CCL2) secretion from retinal pigment epithelia...

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Autores principales: Kohno, Hideo, Terauchi, Ryo, Watanabe, Sumiko, Ichihara, Kosuke, Watanabe, Tomoyuki, Nishijima, Euido, Watanabe, Akira, Nakano, Tadashi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Association for Research in Vision and Ophthalmology 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8590179/
https://www.ncbi.nlm.nih.gov/pubmed/34751741
http://dx.doi.org/10.1167/tvst.10.13.8
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author Kohno, Hideo
Terauchi, Ryo
Watanabe, Sumiko
Ichihara, Kosuke
Watanabe, Tomoyuki
Nishijima, Euido
Watanabe, Akira
Nakano, Tadashi
author_facet Kohno, Hideo
Terauchi, Ryo
Watanabe, Sumiko
Ichihara, Kosuke
Watanabe, Tomoyuki
Nishijima, Euido
Watanabe, Akira
Nakano, Tadashi
author_sort Kohno, Hideo
collection PubMed
description PURPOSE: Although lecithin-bound iodine (LBI) has been administered orally for retinal diseases, a lack of clinical studies and obscure action mechanism of LBI hinder its large-scale prescription. LBI treatment suppresses chemokine (C-C motif) ligand 2 (CCL2) secretion from retinal pigment epithelial cells in vitro. Herein, we assessed the in vivo effect of LBI treatment on retinal degeneration (RD) in mice. METHODS: Mertk(−/−)Cx3cr1(GFP/+)Ccr2(RFP/+) mice—a model for RD—demonstrate fluorescein-labeled microglia/macrophage to facilitate visualization of CX3CR1-green fluorescent protein (GFP) and CCR2-red fluorescent protein (RFP). An LBI-containing mouse diet was provided to Mertk(−/−)Cx3cr1(GFP/+)Ccr2(RFP/+) mice ad libitum from postnatal day (POD) 28. CX3CR1-GFP and CCR2-RFP expression was assessed at POD 56 using retinal sectioning and flat mounting. RD severity was assessed at POD 84. Retinal RNA was extracted from the mice of each group to measure chemokine expression. Electroretinography was performed to assess retinal function. RESULTS: CCR2-RFP expression in the retina and retinal pigment epithelial cells was suppressed by LBI treatment compared with that in the control at POD 56. The number of outer nuclear layer nuclei was higher in the group fed with LBI-containing diet than in the control mice at POD 84. Ccl2 and Ccr2 RNA expression was suppressed by LBI intake. Electroretinography showed the LBI-treated group to have a high b-wave amplitude compared with the control group. CONCLUSIONS: Suppressing CCR2-RFP–positive macrophage invasion into the retina and CCL2 and CCR2 expression is a potential mechanism underlying LBI-mediated attenuation of RD. TRANSLATIONAL RELEVANCE: Life-long LBI administration may become a candidate for treating RD.
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spelling pubmed-85901792021-11-24 Effect of Lecithin-Bound Iodine Treatment on Inherited Retinal Degeneration in Mice Kohno, Hideo Terauchi, Ryo Watanabe, Sumiko Ichihara, Kosuke Watanabe, Tomoyuki Nishijima, Euido Watanabe, Akira Nakano, Tadashi Transl Vis Sci Technol Article PURPOSE: Although lecithin-bound iodine (LBI) has been administered orally for retinal diseases, a lack of clinical studies and obscure action mechanism of LBI hinder its large-scale prescription. LBI treatment suppresses chemokine (C-C motif) ligand 2 (CCL2) secretion from retinal pigment epithelial cells in vitro. Herein, we assessed the in vivo effect of LBI treatment on retinal degeneration (RD) in mice. METHODS: Mertk(−/−)Cx3cr1(GFP/+)Ccr2(RFP/+) mice—a model for RD—demonstrate fluorescein-labeled microglia/macrophage to facilitate visualization of CX3CR1-green fluorescent protein (GFP) and CCR2-red fluorescent protein (RFP). An LBI-containing mouse diet was provided to Mertk(−/−)Cx3cr1(GFP/+)Ccr2(RFP/+) mice ad libitum from postnatal day (POD) 28. CX3CR1-GFP and CCR2-RFP expression was assessed at POD 56 using retinal sectioning and flat mounting. RD severity was assessed at POD 84. Retinal RNA was extracted from the mice of each group to measure chemokine expression. Electroretinography was performed to assess retinal function. RESULTS: CCR2-RFP expression in the retina and retinal pigment epithelial cells was suppressed by LBI treatment compared with that in the control at POD 56. The number of outer nuclear layer nuclei was higher in the group fed with LBI-containing diet than in the control mice at POD 84. Ccl2 and Ccr2 RNA expression was suppressed by LBI intake. Electroretinography showed the LBI-treated group to have a high b-wave amplitude compared with the control group. CONCLUSIONS: Suppressing CCR2-RFP–positive macrophage invasion into the retina and CCL2 and CCR2 expression is a potential mechanism underlying LBI-mediated attenuation of RD. TRANSLATIONAL RELEVANCE: Life-long LBI administration may become a candidate for treating RD. The Association for Research in Vision and Ophthalmology 2021-11-09 /pmc/articles/PMC8590179/ /pubmed/34751741 http://dx.doi.org/10.1167/tvst.10.13.8 Text en Copyright 2021 The Authors https://creativecommons.org/licenses/by/4.0/This work is licensed under a Creative Commons Attribution 4.0 International License.
spellingShingle Article
Kohno, Hideo
Terauchi, Ryo
Watanabe, Sumiko
Ichihara, Kosuke
Watanabe, Tomoyuki
Nishijima, Euido
Watanabe, Akira
Nakano, Tadashi
Effect of Lecithin-Bound Iodine Treatment on Inherited Retinal Degeneration in Mice
title Effect of Lecithin-Bound Iodine Treatment on Inherited Retinal Degeneration in Mice
title_full Effect of Lecithin-Bound Iodine Treatment on Inherited Retinal Degeneration in Mice
title_fullStr Effect of Lecithin-Bound Iodine Treatment on Inherited Retinal Degeneration in Mice
title_full_unstemmed Effect of Lecithin-Bound Iodine Treatment on Inherited Retinal Degeneration in Mice
title_short Effect of Lecithin-Bound Iodine Treatment on Inherited Retinal Degeneration in Mice
title_sort effect of lecithin-bound iodine treatment on inherited retinal degeneration in mice
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8590179/
https://www.ncbi.nlm.nih.gov/pubmed/34751741
http://dx.doi.org/10.1167/tvst.10.13.8
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