Determination of osteopontin in monitoring retinal damage in metabolic syndrome

IF 1.8 4区 医学 Q3 PATHOLOGY
Ramona D'Amico, Rosalba Siracusa, Marika Cordaro, Roberta Fusco, Livia Interdonato, Gianluca Antonio Franco, Salvatore Cuzzocrea, Rosanna Di Paola, Daniela Impellizzeri
{"title":"Determination of osteopontin in monitoring retinal damage in metabolic syndrome","authors":"Ramona D'Amico,&nbsp;Rosalba Siracusa,&nbsp;Marika Cordaro,&nbsp;Roberta Fusco,&nbsp;Livia Interdonato,&nbsp;Gianluca Antonio Franco,&nbsp;Salvatore Cuzzocrea,&nbsp;Rosanna Di Paola,&nbsp;Daniela Impellizzeri","doi":"10.1111/iep.12518","DOIUrl":null,"url":null,"abstract":"<p>Metabolic syndrome (MetS) is becoming an increasing public health challenge. Many of the individual components of MetS are associated with ocular changes, but it is not yet clear what the association is. It is known that MetS can lead to diabetes and hence its consequences such as retinopathy. Osteopontin (OPN) is a phosphoglycoprotein that appears to be implicated in diabetic retinopathy. Given the involvement of OPN in retinal damage, the aim of this research was to evaluate OPN expression and its variation over time in a model of MetS induced by 30% fructose consumption for 1, 2 and 3 months. The weight of the animals and the consumption of food and fructose/water were evaluated during the experiment. The results showed a time-dependent increase in weight and liquid consumption in animals treated with fructose, while there was no significant difference in food consumption. Subsequently, the biochemical parameters confirmed that the animals treated with fructose, over time, underwent alterations like those found in patients with MetS. We then moved on to the evaluation of OPN and microglia. In both cases, we observed a time-dependent increase in OPN and Iba-1 in fructose consumption. Furthermore, the results showed a gradual loss of ZO-1 and occludin levels over time. Thus identification of OPN in patients with MetS could be used as an early marker of retinal damage, and this could help to prevent the complications related to the progression of this pathology.</p>","PeriodicalId":14157,"journal":{"name":"International Journal of Experimental Pathology","volume":"105 6","pages":"206-218"},"PeriodicalIF":1.8000,"publicationDate":"2024-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/iep.12518","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"International Journal of Experimental Pathology","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1111/iep.12518","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"PATHOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Metabolic syndrome (MetS) is becoming an increasing public health challenge. Many of the individual components of MetS are associated with ocular changes, but it is not yet clear what the association is. It is known that MetS can lead to diabetes and hence its consequences such as retinopathy. Osteopontin (OPN) is a phosphoglycoprotein that appears to be implicated in diabetic retinopathy. Given the involvement of OPN in retinal damage, the aim of this research was to evaluate OPN expression and its variation over time in a model of MetS induced by 30% fructose consumption for 1, 2 and 3 months. The weight of the animals and the consumption of food and fructose/water were evaluated during the experiment. The results showed a time-dependent increase in weight and liquid consumption in animals treated with fructose, while there was no significant difference in food consumption. Subsequently, the biochemical parameters confirmed that the animals treated with fructose, over time, underwent alterations like those found in patients with MetS. We then moved on to the evaluation of OPN and microglia. In both cases, we observed a time-dependent increase in OPN and Iba-1 in fructose consumption. Furthermore, the results showed a gradual loss of ZO-1 and occludin levels over time. Thus identification of OPN in patients with MetS could be used as an early marker of retinal damage, and this could help to prevent the complications related to the progression of this pathology.

Abstract Image

在监测代谢综合征视网膜损伤时测定骨蛋白。
代谢综合征(MetS)正日益成为一项公共卫生挑战。代谢综合征的许多单个成分都与眼部变化有关,但目前尚不清楚两者之间的关联是什么。众所周知,代谢综合征可导致糖尿病,进而引发视网膜病变等后果。骨化蛋白(OPN)是一种磷脂酰蛋白,似乎与糖尿病视网膜病变有关。鉴于 OPN 与视网膜损伤的关系,本研究的目的是评估在食用 30% 的果糖 1 个月、2 个月和 3 个月的 MetS 模型中 OPN 的表达及其随时间的变化。实验期间对动物的体重以及食物和果糖/水的消耗量进行了评估。结果显示,使用果糖治疗的动物体重和液体消耗量的增加与时间有关,而食物消耗量则没有显著差异。随后,生化参数证实,接受果糖治疗的动物随着时间的推移会发生与代谢紊乱症患者相同的变化。我们接着评估了 OPN 和小胶质细胞。在这两种情况下,我们都观察到在摄入果糖的情况下,OPN 和 Iba-1 的增加与时间有关。此外,结果还显示,随着时间的推移,ZO-1 和闭塞素的水平会逐渐下降。因此,在 MetS 患者中识别 OPN 可作为视网膜损伤的早期标志物,这有助于预防与这一病理进展相关的并发症。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
CiteScore
4.50
自引率
3.30%
发文量
35
审稿时长
>12 weeks
期刊介绍: Experimental Pathology encompasses the use of multidisciplinary scientific techniques to investigate the pathogenesis and progression of pathologic processes. The International Journal of Experimental Pathology - IJEP - publishes papers which afford new and imaginative insights into the basic mechanisms underlying human disease, including in vitro work, animal models, and clinical research. Aiming to report on work that addresses the common theme of mechanism at a cellular and molecular level, IJEP publishes both original experimental investigations and review articles. Recent themes for review series have covered topics as diverse as "Viruses and Cancer", "Granulomatous Diseases", "Stem cells" and "Cardiovascular Pathology".
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信