老年高压青光眼小鼠炎症加剧

IF 3.7 3区 医学 Q2 GERIATRICS & GERONTOLOGY Neurobiology of Aging Pub Date : 2024-10-09 DOI:10.1016/j.neurobiolaging.2024.10.001
Sabrina Reinehr , M. Rahim Pamuk , Rudolf Fuchshofer , H. Burkhard Dick , Stephanie C. Joachim
{"title":"老年高压青光眼小鼠炎症加剧","authors":"Sabrina Reinehr ,&nbsp;M. Rahim Pamuk ,&nbsp;Rudolf Fuchshofer ,&nbsp;H. Burkhard Dick ,&nbsp;Stephanie C. Joachim","doi":"10.1016/j.neurobiolaging.2024.10.001","DOIUrl":null,"url":null,"abstract":"<div><div>Besides an elevated intraocular pressure (IOP), advanced age is one of the most crucial risk factors for developing glaucoma. βB1-Connective Tissue Growth Factor (βB1-CTGF) high-pressure glaucoma mice were used in this study to assess whether glaucoma mice display more inflammatory and aging processes than age-matched controls. Therefore, 20-month-old βB1-CTGF and corresponding wildtype (WT) controls were examined. After IOP measurements, retinas were processed for (immuno-)histological and quantitative real-time PCR analyses. A significantly higher IOP and diminished retinal ganglion cell numbers were noted in βB1-CTGF mice compared to WT. An enhanced macrogliosis as well as an increased number of microglia/macrophages and microglia was detected in retinas of old glaucoma mice. Interleukin (IL)-1β, IL-6, tumor necrosis factor-α, and transforming growth factor-β2 were upregulated, suggesting an ongoing inflammation. Moreover, βB1-CTGF retinas displayed an increased senescence-associated β-galactosidase staining accompanied by a downregulation of <em>Lmnb1</em> (laminin-B1) mRNA levels. Our results provide a deeper insight into the association between inflammation and high-pressure glaucoma and thus might help to develop new therapy strategies.</div></div>","PeriodicalId":19110,"journal":{"name":"Neurobiology of Aging","volume":"145 ","pages":"Pages 55-64"},"PeriodicalIF":3.7000,"publicationDate":"2024-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Increased inflammation in older high-pressure glaucoma mice\",\"authors\":\"Sabrina Reinehr ,&nbsp;M. Rahim Pamuk ,&nbsp;Rudolf Fuchshofer ,&nbsp;H. Burkhard Dick ,&nbsp;Stephanie C. Joachim\",\"doi\":\"10.1016/j.neurobiolaging.2024.10.001\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>Besides an elevated intraocular pressure (IOP), advanced age is one of the most crucial risk factors for developing glaucoma. βB1-Connective Tissue Growth Factor (βB1-CTGF) high-pressure glaucoma mice were used in this study to assess whether glaucoma mice display more inflammatory and aging processes than age-matched controls. Therefore, 20-month-old βB1-CTGF and corresponding wildtype (WT) controls were examined. After IOP measurements, retinas were processed for (immuno-)histological and quantitative real-time PCR analyses. A significantly higher IOP and diminished retinal ganglion cell numbers were noted in βB1-CTGF mice compared to WT. An enhanced macrogliosis as well as an increased number of microglia/macrophages and microglia was detected in retinas of old glaucoma mice. Interleukin (IL)-1β, IL-6, tumor necrosis factor-α, and transforming growth factor-β2 were upregulated, suggesting an ongoing inflammation. Moreover, βB1-CTGF retinas displayed an increased senescence-associated β-galactosidase staining accompanied by a downregulation of <em>Lmnb1</em> (laminin-B1) mRNA levels. Our results provide a deeper insight into the association between inflammation and high-pressure glaucoma and thus might help to develop new therapy strategies.</div></div>\",\"PeriodicalId\":19110,\"journal\":{\"name\":\"Neurobiology of Aging\",\"volume\":\"145 \",\"pages\":\"Pages 55-64\"},\"PeriodicalIF\":3.7000,\"publicationDate\":\"2024-10-09\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Neurobiology of Aging\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0197458024001702\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"GERIATRICS & GERONTOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neurobiology of Aging","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0197458024001702","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"GERIATRICS & GERONTOLOGY","Score":null,"Total":0}
引用次数: 0

摘要

除了眼内压(IOP)升高外,高龄也是罹患青光眼的最关键风险因素之一。本研究利用βB1-结缔组织生长因子(βB1-CTGF)高压青光眼小鼠来评估青光眼小鼠是否比年龄匹配的对照组表现出更多的炎症和衰老过程。因此,研究人员对 20 个月大的βB1-CTGF 小鼠和相应的野生型(WT)对照组进行了检查。测量眼压后,对视网膜进行(免疫)组织学和实时定量 PCR 分析。与 WT 相比,βB1-CTGF 小鼠的眼压明显升高,视网膜神经节细胞数量减少。在老年性青光眼小鼠的视网膜中,检测到大胶质细胞增多以及小胶质细胞/巨噬细胞和小胶质细胞数量增加。白细胞介素(IL)-1β、IL-6、肿瘤坏死因子-α和转化生长因子-β2上调,表明炎症正在持续。此外,βB1-CTGF 视网膜显示衰老相关的 β-半乳糖苷酶染色增加,同时 Lmnb1(层粘连蛋白-B1)mRNA 水平下调。我们的研究结果让我们更深入地了解了炎症与高压性青光眼之间的关联,从而可能有助于开发新的治疗策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
Increased inflammation in older high-pressure glaucoma mice
Besides an elevated intraocular pressure (IOP), advanced age is one of the most crucial risk factors for developing glaucoma. βB1-Connective Tissue Growth Factor (βB1-CTGF) high-pressure glaucoma mice were used in this study to assess whether glaucoma mice display more inflammatory and aging processes than age-matched controls. Therefore, 20-month-old βB1-CTGF and corresponding wildtype (WT) controls were examined. After IOP measurements, retinas were processed for (immuno-)histological and quantitative real-time PCR analyses. A significantly higher IOP and diminished retinal ganglion cell numbers were noted in βB1-CTGF mice compared to WT. An enhanced macrogliosis as well as an increased number of microglia/macrophages and microglia was detected in retinas of old glaucoma mice. Interleukin (IL)-1β, IL-6, tumor necrosis factor-α, and transforming growth factor-β2 were upregulated, suggesting an ongoing inflammation. Moreover, βB1-CTGF retinas displayed an increased senescence-associated β-galactosidase staining accompanied by a downregulation of Lmnb1 (laminin-B1) mRNA levels. Our results provide a deeper insight into the association between inflammation and high-pressure glaucoma and thus might help to develop new therapy strategies.
求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Neurobiology of Aging
Neurobiology of Aging 医学-老年医学
CiteScore
8.40
自引率
2.40%
发文量
225
审稿时长
67 days
期刊介绍: Neurobiology of Aging publishes the results of studies in behavior, biochemistry, cell biology, endocrinology, molecular biology, morphology, neurology, neuropathology, pharmacology, physiology and protein chemistry in which the primary emphasis involves mechanisms of nervous system changes with age or diseases associated with age. Reviews and primary research articles are included, occasionally accompanied by open peer commentary. Letters to the Editor and brief communications are also acceptable. Brief reports of highly time-sensitive material are usually treated as rapid communications in which case editorial review is completed within six weeks and publication scheduled for the next available issue.
期刊最新文献
Cerebral white matter hyperintensity volumes: Normative age- and sex-specific values from 15 population-based cohorts comprising 14,876 individuals Contents Editorial Advisory Board Cross-sectional and longitudinal relationships among blood-brain barrier disruption, Alzheimer's disease biomarkers, and cognition in cognitively normal older adults Effects of age and dietary methionine restriction on cognitive and behavioural phenotypes in the rTg4510 mouse model of frontotemporal dementia
×
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
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 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 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1