脂肪酸去饱和酶1敲低促进糖尿病角膜上皮的创面愈合和功能恢复。

IF 4.7 2区 医学 Q1 OPHTHALMOLOGY
Yangqi Zhao, Yi Dong, Qingqing Zheng, Yue Zhao, Yingjie Ni, Peijin Qiu, Chuannan Chen, Mengyue Xu, Chaoyang Hong, Ting Shen
{"title":"脂肪酸去饱和酶1敲低促进糖尿病角膜上皮的创面愈合和功能恢复。","authors":"Yangqi Zhao, Yi Dong, Qingqing Zheng, Yue Zhao, Yingjie Ni, Peijin Qiu, Chuannan Chen, Mengyue Xu, Chaoyang Hong, Ting Shen","doi":"10.1167/iovs.66.6.6","DOIUrl":null,"url":null,"abstract":"<p><strong>Purpose: </strong>Fatty acid desaturase 1 (FADS1) is significantly and specifically upregulated following diabetic corneal injury. However, its role in diabetic keratopathy remains unclear. This study aimed to investigate the impact of FADS1 on wound healing and functional recovery of the diabetic corneal epithelium and explore its potential mechanisms.</p><p><strong>Methods: </strong>Using high-glucose-induced corneal epithelial cells and a streptozotocin-induced type 1 diabetic mouse model, FADS1 expression was suppressed via FADS1 small interfering RNA (siRNA). Cell migration was assessed using scratch and transwell assays. Wound healing and functional recovery of the corneal epithelium were evaluated using sodium fluorescein staining, anterior segment optical coherence tomography, hematoxylin and eosin staining, and immunofluorescence staining.</p><p><strong>Results: </strong>FADS1 knockdown promoted wound healing and functional recovery of the diabetic corneal epithelium both in vivo and in vitro. Suppression of FADS1 enhanced high-glucose-induced corneal epithelial cell migration, which was dependent on elevated levels of the upstream metabolite γ-linolenic acid. This effect was mediated through the activation of the mitogen-activated protein kinase signaling pathway and the accumulation of autophagosomes.</p><p><strong>Conclusions: </strong>After diabetic corneal epithelial injury, FADS1 expression is specifically upregulated. Knockdown of FADS1 promotes wound healing and functional recovery, suggesting a novel therapeutic strategy for diabetic keratopathy.</p>","PeriodicalId":14620,"journal":{"name":"Investigative ophthalmology & visual science","volume":"66 6","pages":"6"},"PeriodicalIF":4.7000,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12136103/pdf/","citationCount":"0","resultStr":"{\"title\":\"Fatty Acid Desaturase 1 Knockdown Promotes Wound Healing and Functional Recovery of the Corneal Epithelium in Diabetes.\",\"authors\":\"Yangqi Zhao, Yi Dong, Qingqing Zheng, Yue Zhao, Yingjie Ni, Peijin Qiu, Chuannan Chen, Mengyue Xu, Chaoyang Hong, Ting Shen\",\"doi\":\"10.1167/iovs.66.6.6\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Purpose: </strong>Fatty acid desaturase 1 (FADS1) is significantly and specifically upregulated following diabetic corneal injury. However, its role in diabetic keratopathy remains unclear. This study aimed to investigate the impact of FADS1 on wound healing and functional recovery of the diabetic corneal epithelium and explore its potential mechanisms.</p><p><strong>Methods: </strong>Using high-glucose-induced corneal epithelial cells and a streptozotocin-induced type 1 diabetic mouse model, FADS1 expression was suppressed via FADS1 small interfering RNA (siRNA). Cell migration was assessed using scratch and transwell assays. Wound healing and functional recovery of the corneal epithelium were evaluated using sodium fluorescein staining, anterior segment optical coherence tomography, hematoxylin and eosin staining, and immunofluorescence staining.</p><p><strong>Results: </strong>FADS1 knockdown promoted wound healing and functional recovery of the diabetic corneal epithelium both in vivo and in vitro. Suppression of FADS1 enhanced high-glucose-induced corneal epithelial cell migration, which was dependent on elevated levels of the upstream metabolite γ-linolenic acid. This effect was mediated through the activation of the mitogen-activated protein kinase signaling pathway and the accumulation of autophagosomes.</p><p><strong>Conclusions: </strong>After diabetic corneal epithelial injury, FADS1 expression is specifically upregulated. Knockdown of FADS1 promotes wound healing and functional recovery, suggesting a novel therapeutic strategy for diabetic keratopathy.</p>\",\"PeriodicalId\":14620,\"journal\":{\"name\":\"Investigative ophthalmology & visual science\",\"volume\":\"66 6\",\"pages\":\"6\"},\"PeriodicalIF\":4.7000,\"publicationDate\":\"2025-06-02\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12136103/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Investigative ophthalmology & visual science\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1167/iovs.66.6.6\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"OPHTHALMOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Investigative ophthalmology & visual science","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1167/iovs.66.6.6","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"OPHTHALMOLOGY","Score":null,"Total":0}
引用次数: 0

摘要

目的:脂肪酸去饱和酶1 (FADS1)在糖尿病角膜损伤后显著特异性上调。然而,其在糖尿病性角膜病变中的作用尚不清楚。本研究旨在探讨FADS1对糖尿病角膜上皮创面愈合和功能恢复的影响,并探讨其可能的机制。方法:利用高糖诱导的角膜上皮细胞和链脲佐菌素诱导的1型糖尿病小鼠模型,通过FADS1小干扰RNA (siRNA)抑制FADS1的表达。采用划痕法和transwell法评估细胞迁移。采用荧光素钠染色、前段光学相干断层扫描、苏木精和伊红染色和免疫荧光染色评估角膜上皮的伤口愈合和功能恢复情况。结果:FADS1基因敲除在体内和体外均能促进糖尿病角膜上皮创面愈合和功能恢复。抑制FADS1增强了高糖诱导的角膜上皮细胞迁移,这依赖于上游代谢物γ-亚麻酸水平的升高。这种作用是通过丝裂原激活的蛋白激酶信号通路的激活和自噬体的积累介导的。结论:糖尿病角膜上皮损伤后,FADS1表达特异性上调。FADS1基因敲低可促进创面愈合和功能恢复,为糖尿病性角膜病变提供了一种新的治疗策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Fatty Acid Desaturase 1 Knockdown Promotes Wound Healing and Functional Recovery of the Corneal Epithelium in Diabetes.

Purpose: Fatty acid desaturase 1 (FADS1) is significantly and specifically upregulated following diabetic corneal injury. However, its role in diabetic keratopathy remains unclear. This study aimed to investigate the impact of FADS1 on wound healing and functional recovery of the diabetic corneal epithelium and explore its potential mechanisms.

Methods: Using high-glucose-induced corneal epithelial cells and a streptozotocin-induced type 1 diabetic mouse model, FADS1 expression was suppressed via FADS1 small interfering RNA (siRNA). Cell migration was assessed using scratch and transwell assays. Wound healing and functional recovery of the corneal epithelium were evaluated using sodium fluorescein staining, anterior segment optical coherence tomography, hematoxylin and eosin staining, and immunofluorescence staining.

Results: FADS1 knockdown promoted wound healing and functional recovery of the diabetic corneal epithelium both in vivo and in vitro. Suppression of FADS1 enhanced high-glucose-induced corneal epithelial cell migration, which was dependent on elevated levels of the upstream metabolite γ-linolenic acid. This effect was mediated through the activation of the mitogen-activated protein kinase signaling pathway and the accumulation of autophagosomes.

Conclusions: After diabetic corneal epithelial injury, FADS1 expression is specifically upregulated. Knockdown of FADS1 promotes wound healing and functional recovery, suggesting a novel therapeutic strategy for diabetic keratopathy.

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
CiteScore
6.90
自引率
4.50%
发文量
339
审稿时长
1 months
期刊介绍: Investigative Ophthalmology & Visual Science (IOVS), published as ready online, is a peer-reviewed academic journal of the Association for Research in Vision and Ophthalmology (ARVO). IOVS features original research, mostly pertaining to clinical and laboratory ophthalmology and vision research in general.
×
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:604180095
Book学术官方微信