感觉神经在小鼠角膜表型维持中的重要作用。

IF 5.6 1区 医学 Q1 OPHTHALMOLOGY
Yuka Okada , Takayoshi Sumioka , Hiroki Iwanishi , Shingo Yasuda , Jianhua Zhang , Yong Yuan , Chia-Yang Liu , Winston Whei-Yang Kao , Shizuya Saika
{"title":"感觉神经在小鼠角膜表型维持中的重要作用。","authors":"Yuka Okada ,&nbsp;Takayoshi Sumioka ,&nbsp;Hiroki Iwanishi ,&nbsp;Shingo Yasuda ,&nbsp;Jianhua Zhang ,&nbsp;Yong Yuan ,&nbsp;Chia-Yang Liu ,&nbsp;Winston Whei-Yang Kao ,&nbsp;Shizuya Saika","doi":"10.1016/j.jtos.2025.02.012","DOIUrl":null,"url":null,"abstract":"<div><h3>Purpose</h3><div>To the best of our knowledge, no reports have been published on the long-term changes in corneal tissue during the course of neuroparalytic keratopathy caused by destruction of the ophthalmic nerve in experimental animals. To bridge this research gap, we investigated the histopathology of the cornea in mice 3, 12, and 24 months after coagulation of the ophthalmic nerve.</div></div><div><h3>Methods</h3><div>Nerves were severely coagulated by inserting an 18-gauge bipolar needle into the skull of C57Bl/6 mice, as previously reported. Mice were sacrificed 3, 12, and 24 months later. Eyes were processed for histological and immunohistochemical analyses to identify the phenotypes of corneal epithelium and stroma.</div></div><div><h3>Results</h3><div>At 3 months after denervation, the affected eyes showed severe inflammation and epithelial damage. In 3-, 14- and 24-month-old corneas, the stroma was found to be hypercellular with stromal neovascularization and keratinized epithelial hyperplasia. Such epithelium no longer expressed keratin 12, but markedly featured keratinization markers. The affected stroma had no keratocan expression, indicating loss of keratocyte cell-type differentiation. Neutrophils, macrophages, and Sox10-positive putative Schwann cells were found distributed in the affected stroma in association with the accumulation of Sonic hedgehog and galectin-3.</div></div><div><h3>Conclusions</h3><div>Ophthalmic denervation causes prolonged inflammation lasting up to 2 years, the appearance of repair-type Schwann cells in the stroma, loss of cornea-type differentiation of the epithelium with keratinization, and loss of stroma-specific gene expression. Sonic hedgehog and galectin-3 are upregulated in tissues and thought to be involved in pathology.</div></div>","PeriodicalId":54691,"journal":{"name":"Ocular Surface","volume":"37 ","pages":"Pages 80-96"},"PeriodicalIF":5.6000,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Essential roles of sensory nerve in maintenance of cornea-phenotype in mice\",\"authors\":\"Yuka Okada ,&nbsp;Takayoshi Sumioka ,&nbsp;Hiroki Iwanishi ,&nbsp;Shingo Yasuda ,&nbsp;Jianhua Zhang ,&nbsp;Yong Yuan ,&nbsp;Chia-Yang Liu ,&nbsp;Winston Whei-Yang Kao ,&nbsp;Shizuya Saika\",\"doi\":\"10.1016/j.jtos.2025.02.012\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><h3>Purpose</h3><div>To the best of our knowledge, no reports have been published on the long-term changes in corneal tissue during the course of neuroparalytic keratopathy caused by destruction of the ophthalmic nerve in experimental animals. To bridge this research gap, we investigated the histopathology of the cornea in mice 3, 12, and 24 months after coagulation of the ophthalmic nerve.</div></div><div><h3>Methods</h3><div>Nerves were severely coagulated by inserting an 18-gauge bipolar needle into the skull of C57Bl/6 mice, as previously reported. Mice were sacrificed 3, 12, and 24 months later. Eyes were processed for histological and immunohistochemical analyses to identify the phenotypes of corneal epithelium and stroma.</div></div><div><h3>Results</h3><div>At 3 months after denervation, the affected eyes showed severe inflammation and epithelial damage. In 3-, 14- and 24-month-old corneas, the stroma was found to be hypercellular with stromal neovascularization and keratinized epithelial hyperplasia. Such epithelium no longer expressed keratin 12, but markedly featured keratinization markers. The affected stroma had no keratocan expression, indicating loss of keratocyte cell-type differentiation. Neutrophils, macrophages, and Sox10-positive putative Schwann cells were found distributed in the affected stroma in association with the accumulation of Sonic hedgehog and galectin-3.</div></div><div><h3>Conclusions</h3><div>Ophthalmic denervation causes prolonged inflammation lasting up to 2 years, the appearance of repair-type Schwann cells in the stroma, loss of cornea-type differentiation of the epithelium with keratinization, and loss of stroma-specific gene expression. Sonic hedgehog and galectin-3 are upregulated in tissues and thought to be involved in pathology.</div></div>\",\"PeriodicalId\":54691,\"journal\":{\"name\":\"Ocular Surface\",\"volume\":\"37 \",\"pages\":\"Pages 80-96\"},\"PeriodicalIF\":5.6000,\"publicationDate\":\"2025-03-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Ocular Surface\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S1542012425000357\",\"RegionNum\":1,\"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":"Ocular Surface","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1542012425000357","RegionNum":1,"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:据我们所知,尚无关于实验动物眼神经破坏引起的神经麻痹性角膜病变过程中角膜组织长期变化的报道。为了弥补这一研究空白,我们研究了眼神经凝固后3、12和24个月小鼠角膜的组织病理学。方法:根据文献报道,将18号双极针插入C57Bl/6小鼠颅骨,使神经严重凝固。3、12、24个月后处死小鼠。对眼睛进行组织学和免疫组织化学分析,以确定角膜上皮和基质的表型。结果:去神经支配术后3个月,患眼出现严重炎症和上皮损伤。在3、14和24个月大的角膜中,发现间质细胞增多,伴有间质新生血管和角化上皮增生。这种上皮不再表达角蛋白12,但明显具有角化标志物。受影响的基质没有角质蛋白表达,表明角质细胞类型分化的丧失。中性粒细胞、巨噬细胞和推测的sox10阳性雪旺细胞分布在受影响的基质中,与Sonic hedgehog和半乳糖凝集素-3的积累有关。结论:眼球去神经支配可引起长达2年的长期炎症,在基质中出现修复型雪旺细胞,角膜上皮的角膜型分化丧失,并伴有角化,基质特异性基因表达丧失。Sonic hedgehog和半乳糖凝集素-3在组织中表达上调,被认为与病理有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Essential roles of sensory nerve in maintenance of cornea-phenotype in mice

Purpose

To the best of our knowledge, no reports have been published on the long-term changes in corneal tissue during the course of neuroparalytic keratopathy caused by destruction of the ophthalmic nerve in experimental animals. To bridge this research gap, we investigated the histopathology of the cornea in mice 3, 12, and 24 months after coagulation of the ophthalmic nerve.

Methods

Nerves were severely coagulated by inserting an 18-gauge bipolar needle into the skull of C57Bl/6 mice, as previously reported. Mice were sacrificed 3, 12, and 24 months later. Eyes were processed for histological and immunohistochemical analyses to identify the phenotypes of corneal epithelium and stroma.

Results

At 3 months after denervation, the affected eyes showed severe inflammation and epithelial damage. In 3-, 14- and 24-month-old corneas, the stroma was found to be hypercellular with stromal neovascularization and keratinized epithelial hyperplasia. Such epithelium no longer expressed keratin 12, but markedly featured keratinization markers. The affected stroma had no keratocan expression, indicating loss of keratocyte cell-type differentiation. Neutrophils, macrophages, and Sox10-positive putative Schwann cells were found distributed in the affected stroma in association with the accumulation of Sonic hedgehog and galectin-3.

Conclusions

Ophthalmic denervation causes prolonged inflammation lasting up to 2 years, the appearance of repair-type Schwann cells in the stroma, loss of cornea-type differentiation of the epithelium with keratinization, and loss of stroma-specific gene expression. Sonic hedgehog and galectin-3 are upregulated in tissues and thought to be involved in pathology.
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
Ocular Surface
Ocular Surface 医学-眼科学
CiteScore
11.60
自引率
14.10%
发文量
97
审稿时长
39 days
期刊介绍: The Ocular Surface, a quarterly, a peer-reviewed journal, is an authoritative resource that integrates and interprets major findings in diverse fields related to the ocular surface, including ophthalmology, optometry, genetics, molecular biology, pharmacology, immunology, infectious disease, and epidemiology. Its critical review articles cover the most current knowledge on medical and surgical management of ocular surface pathology, new understandings of ocular surface physiology, the meaning of recent discoveries on how the ocular surface responds to injury and disease, and updates on drug and device development. The journal also publishes select original research reports and articles describing cutting-edge techniques and technology in the field. Benefits to authors We also provide many author benefits, such as free PDFs, a liberal copyright policy, special discounts on Elsevier publications and much more. Please click here for more information on our author services. Please see our Guide for Authors for information on article submission. If you require any further information or help, please visit our Support Center
×
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