Effect of Lecithin-Bound Iodine Treatment on Inherited Retinal Degeneration in Mice.
Effect of Lecithin-Bound Iodine Treatment on Inherited Retinal Degeneration in Mice.
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DOI：
10.1167/tvst.10.13.8
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发表时间：
2021-11-01
影响因子：
3
通讯作者：
Nakano T
中科院分区：
文献类型：
--
作者：
Kohno H;Terauchi R;Watanabe S;Ichihara K;Watanabe T;Nishijima E;Watanabe A;Nakano T
虽然卵磷脂结合碘(LBI)已被用于治疗视网膜疾病，但由于缺乏临床研究，其作用机制尚不清楚，阻碍了其规模化处方。LBI抑制体外培养的视网膜色素上皮细胞分泌趋化因子(C-C基序)配体2(CCL2)。在此，我们评估了LBI治疗对小鼠视网膜变性(RD)的体内效应。MerTK−/−Cx3cr1GFP/+Ccr2RFP/+小鼠--一种RD模型--展示了荧光素标记的小胶质细胞/巨噬细胞，以促进CX3CR1-绿色荧光蛋白和CCR2-红色荧光蛋白的可视化。MerTK−/−Cx3cr1GFP/+Ccr2RFP/+小鼠从出生后28天起随机给予含LBI的小鼠饲料。用视网膜切片和平板贴壁法在POD 56时评估CX3CR1-GFP和CCR2-RFP的表达。在POD 84分时评估RD的严重程度。提取各组小鼠视网膜RNA，检测趋化因子的表达。进行视网膜电流图检查以评估视网膜功能。LBI处理组大鼠视网膜和视网膜色素上皮细胞CCR2-RFP的表达在POD 56时较对照组明显降低。在第84天，饲喂含LBI饲料的小鼠外核层核数高于对照组。摄入LBI可抑制CCL2和CCR2的RNA表达。视网膜电图显示LBI治疗组与对照组相比，b波波幅较高。抑制CCR2-RFP阳性的巨噬细胞对视网膜的侵袭以及CCL2和CCR2的表达是LBI介导的RD减弱的一个潜在机制。终生LBI治疗可能成为治疗RD的候选药物。
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. Mertk−/−Cx3cr1GFP/+Ccr2RFP/+ 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−/−Cx3cr1GFP/+Ccr2RFP/+ 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. 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. Suppressing CCR2-RFP–positive macrophage invasion into the retina and CCL2 and CCR2 expression is a potential mechanism underlying LBI-mediated attenuation of RD. Life-long LBI administration may become a candidate for treating RD.
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影响因子：
8.1
作者：
Sandberg, Michael A.;Pearce, Elizabeth N.;Berson, Eliot L.
通讯作者：
Berson, Eliot L.
影响因子：
9.3
作者：
Kohno H;Koso H;Okano K;Sundermeier TR;Saito S;Watanabe S;Tsuneoka H;Sakai T
通讯作者：
Sakai T
DOI：
10.1007/bf00684829
发表时间：
1957-01-01
期刊：
Albrecht von Graefe's Archiv fur Ophthalmologie
影响因子：
--
作者：
TRICHTEL, F
通讯作者：
TRICHTEL, F
影响因子：
5.6
作者：
Ashok A;Singh N;Chaudhary S;Bellamkonda V;Kritikos AE;Wise AS;Rana N;McDonald D;Ayyagari R
通讯作者：
Ayyagari R
DOI：
10.4049/jimmunol.1301738
发表时间：
2014-04-15
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Kohno H;Maeda T;Perusek L;Pearlman E;Maeda A
通讯作者：
Maeda A