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作 者:Wei Xu Li-Jin Cui Xiao-Ying Yang Xiao-Yuan Cui Jian Guo Guo-Xing Xu
机构地区:[1]Department of Ophthalmology,the First Affiliated Hospital of Fujian Medical University,Fuzhou 350001,Fujian Province,China [2]Department of Ophthalmology,National Regional Medical Center,Binhai Campus of the First Affiliated Hospital of Fujian Medical University,Fuzhou 350212,Fujian Province,China [3]Fujian Institute of Ophthalmology,Fuzhou 350001,Fujian Province,China
出 处:《International Journal of Ophthalmology(English edition)》2024年第10期1800-1808,共9页国际眼科杂志(英文版)
基 金:Supported by National Natural Science Foundation of China(No.81900862)。
摘 要: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 receptorβ(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 PDGFRβwere 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:PDGFRβblockage 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 PDGFRβblockage group.Fur ther upregulation of cytokines monocyte chemoattractant protein 1(MCP-1)and interleukin-1β(IL-1β)was also observed following PDGFRβinhibition.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,PDGFRβblockage in retinal pericytes abolished these cellular responses to light-induced damage,consistent with the in vivo PDGFRβblockage 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.
关 键 词:PERICYTE Müller glia light-induced retinal injury platelet-derived growth factor receptorβ signal pathway
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