在光诱导视网膜损伤的啮齿动物模型中,通过抑制 PDGFRβ 而受损的周细胞与缪勒神经胶质细胞之间的相互作用加剧了光感受器的丧失。

IF 1.9 4区 医学 Q2 OPHTHALMOLOGY
International journal of ophthalmology Pub Date : 2024-10-18 eCollection Date: 2024-01-01 DOI:10.18240/ijo.2024.10.05
Wei Xu, Li-Jin Cui, Xiao-Ying Yang, Xiao-Yuan Cui, Jian Guo, Guo-Xing Xu
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引用次数: 0

摘要

目的:研究视网膜周细胞-Müller胶质细胞相互作用在视网膜损伤修复中的参与,并评估抑制视网膜周细胞血小板衍生生长因子受体β(PDGFRβ)信号通路对感光细胞损失和Müller胶质细胞反应的影响:方法:将 Sprague-Dawley 大鼠暴露于强光下诱导视网膜损伤。方法:将 Sprague-Dawley 大鼠暴露于强光下诱导视网膜损伤,通过玻璃体内注射中和 PDGFRβ 抗体阻断视网膜周细胞的信号通路。对光损伤后的视网膜组织学和Müller神经胶质反应进行了评估。在体外,正常视网膜周细胞和PDGFRβ阻断的视网膜周细胞与Müller细胞系(rMC-1)共同培养,以检测补充光损伤的匀浆视网膜(SHRs)上清液后的形态和蛋白表达变化:结果:在强光照射前24小时阻断PDGFRβ会显著加剧感光细胞的丧失。强光照射后观察到的 GFAP 和 p-STAT3 的上调在 PDGFRβ 阻断组中得到显著抑制。在抑制 PDGFRβ 后,还观察到细胞因子单核细胞趋化蛋白 1(MCP-1)和白细胞介素-1β(IL-1β)进一步上调。在体外共培养系统中,加入光损伤的 SHRs 会诱导周细胞变形和增殖细胞核抗原(PCNA)表达上调,而 Müller 细胞则表现出神经元样形态并表达 Nestin。然而,阻断视网膜周细胞中的PDGFRβ可消除这些细胞对光诱导损伤的反应,这与体内PDGFRβ阻断的结果一致:结论:视网膜周细胞与缪勒神经胶质细胞的相互作用在视网膜损伤的内源性修复过程中发挥着潜在作用。结论:在视网膜损伤的内源性修复过程中,周细胞-缪勒神经胶质细胞的相互作用发挥着潜在的作用,这种相互作用的损害会加剧光诱导的视网膜损伤中感光细胞的退化。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Impaired pericyte-Müller glia interaction via PDGFRβ suppression aggravates photoreceptor loss in a rodent model of light-induced retinal injury.

Aim: To investigate the involvement of pericyte-Müller glia interaction in retinal damage repair and assess the influence of suppressing the platelet-derived growth factor receptor β (PDGFRβ) signaling pathway in retinal pericytes on photoreceptor loss and Müller glial response.

Methods: Sprague-Dawley rats were exposed to intense light to induce retinal injury. Neutralizing antibody against PDGFRβ were deployed to block the signaling pathway in retinal pericytes through intravitreal injection. Retinal histology and Müller glial reaction were assessed following light injury. In vitro, normal and PDGFRβ-blocked retinal pericytes were cocultured with Müller cell line (rMC-1) to examine morphological and protein expression changes upon supplementation with light-injured supernatants of homogenized retinas (SHRs).

Results: PDGFRβ blockage 24h prior to intense light exposure resulted in a significant exacerbation of photoreceptor loss. The upregulation of GFAP and p-STAT3, observed after intense light exposure, was significantly inhibited in the PDGFRβ blockage group. Further upregulation of cytokines monocyte chemoattractant protein 1 (MCP-1) and interleukin-1β (IL-1β) was also observed following PDGFRβ inhibition. In the in vitro coculture system, the addition of light-injured SHRs induced pericyte deformation and upregulation of proliferating cell nuclear antigen (PCNA) expression, while Müller cells exhibited neuron-like morphology and expressed Nestin. However, PDGFRβ blockage in retinal pericytes abolished these cellular responses to light-induced damage, consistent with the in vivo PDGFRβ blockage findings.

Conclusion: Pericyte-Müller glia interaction plays a potential role in the endogenous repair process of retinal injury. Impairment of this interaction exacerbates photoreceptor degeneration in light-induced retinal injury.

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来源期刊
CiteScore
2.50
自引率
7.10%
发文量
3141
审稿时长
4-8 weeks
期刊介绍: · International Journal of Ophthalmology-IJO (English edition) is a global ophthalmological scientific publication and a peer-reviewed open access periodical (ISSN 2222-3959 print, ISSN 2227-4898 online). This journal is sponsored by Chinese Medical Association Xi’an Branch and obtains guidance and support from WHO and ICO (International Council of Ophthalmology). It has been indexed in SCIE, PubMed, PubMed-Central, Chemical Abstracts, Scopus, EMBASE , and DOAJ. IJO JCR IF in 2017 is 1.166. IJO was established in 2008, with editorial office in Xi’an, China. It is a monthly publication. General Scientific Advisors include Prof. Hugh Taylor (President of ICO); Prof.Bruce Spivey (Immediate Past President of ICO); Prof.Mark Tso (Ex-Vice President of ICO) and Prof.Daiming Fan (Academician and Vice President, Chinese Academy of Engineering. International Scientific Advisors include Prof. Serge Resnikoff (WHO Senior Speciatist for Prevention of blindness), Prof. Chi-Chao Chan (National Eye Institute, USA) and Prof. Richard L Abbott (Ex-President of AAO/PAAO) et al. Honorary Editors-in-Chief: Prof. Li-Xin Xie(Academician of Chinese Academy of Engineering/Honorary President of Chinese Ophthalmological Society); Prof. Dennis Lam (President of APAO) and Prof. Xiao-Xin Li (Ex-President of Chinese Ophthalmological Society). Chief Editor: Prof. Xiu-Wen Hu (President of IJO Press). Editors-in-Chief: Prof. Yan-Nian Hui (Ex-Director, Eye Institute of Chinese PLA) and Prof. George Chiou (Founding chief editor of Journal of Ocular Pharmacology & Therapeutics). Associate Editors-in-Chief include: Prof. Ning-Li Wang (President Elect of APAO); Prof. Ke Yao (President of Chinese Ophthalmological Society) ; Prof.William Smiddy (Bascom Palmer Eye instituteUSA) ; Prof.Joel Schuman (President of Association of University Professors of Ophthalmology,USA); Prof.Yizhi Liu (Vice President of Chinese Ophtlalmology Society); Prof.Yu-Sheng Wang (Director of Eye Institute of Chinese PLA); Prof.Ling-Yun Cheng (Director of Ocular Pharmacology, Shiley Eye Center, USA). IJO accepts contributions in English from all over the world. It includes mainly original articles and review articles, both basic and clinical papers. Instruction is Welcome Contribution is Welcome Citation is Welcome Cooperation organization International Council of Ophthalmology(ICO), PubMed, PMC, American Academy of Ophthalmology, Asia-Pacific, Thomson Reuters, The Charlesworth Group, Crossref,Scopus,Publons, DOAJ etc.
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