{"title":"Impaired pericyte-Müller glia interaction <i>via</i> PDGFRβ suppression aggravates photoreceptor loss in a rodent model of light-induced retinal injury.","authors":"Wei Xu, Li-Jin Cui, Xiao-Ying Yang, Xiao-Yuan Cui, Jian Guo, Guo-Xing Xu","doi":"10.18240/ijo.2024.10.05","DOIUrl":null,"url":null,"abstract":"<p><strong>Aim: </strong>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.</p><p><strong>Methods: </strong>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. <i>In vitro</i>, 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).</p><p><strong>Results: </strong>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 <i>in vitro</i> 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 <i>in vivo</i> PDGFRβ blockage findings.</p><p><strong>Conclusion: </strong>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.</p>","PeriodicalId":14312,"journal":{"name":"International journal of ophthalmology","volume":null,"pages":null},"PeriodicalIF":1.9000,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11422380/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"International journal of ophthalmology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.18240/ijo.2024.10.05","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"OPHTHALMOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
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.
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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