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miR-26a-5p调控PTEN/PI3K/Akt信号通路对高糖诱导视网膜Müller细胞活化及凋亡的影响
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作者 唐德荣 杨雨雯 +1 位作者 石蕊 刘丹丹 《西安交通大学学报(医学版)》 CAS CSCD 北大核心 2024年第5期705-711,共7页
目的检测微小RNA-26a-5p(microRNA-26a-5p,miR-26a-5p)对PTEN/PI3K/Akt信号通路及高糖刺激的视网膜Müller细胞凋亡的影响,探讨糖尿病视网膜神经损伤的潜在机制。方法采用不同浓度的葡萄糖刺激视网膜Müller细胞构建糖尿病视网... 目的检测微小RNA-26a-5p(microRNA-26a-5p,miR-26a-5p)对PTEN/PI3K/Akt信号通路及高糖刺激的视网膜Müller细胞凋亡的影响,探讨糖尿病视网膜神经损伤的潜在机制。方法采用不同浓度的葡萄糖刺激视网膜Müller细胞构建糖尿病视网膜神经损伤模型,采用CCK-8及流式细胞仪观察细胞增殖及凋亡情况,细胞转染过表达miR-26a-5p模拟物,Real-time PCR检测miR-26a-5p、PTEN、PI3K、Akt的表达情况,ELISA测定细胞上清液中IL-1β及IL-6的水平,采用Graphpad 8.0软件处理数据。结果高糖刺激视网膜Müller细胞生长活跃,与对照组相比,50 mmol/L高糖刺激Müller细胞活力在12 h、24 h时逐渐增加,48 h时活力减弱,细胞凋亡增加,组间差异有统计学意义(P<0.05)。高糖刺激后视网膜Müller细胞中miR-26a-5p水平下降,PTEN的表达显著升高,PI3K及Akt水平下降,IL-1β及IL-6的水平明显升高,过表达miR-26a-5p后,PTEN水平降低,PI3K/Akt及炎性因子降低,细胞凋亡减少(P<0.01)。结论miR-26a-5p通过调控PTEN/PI3K/Akt的表达,影响炎症因子释放,减轻高糖诱导的视网膜Müller细胞凋亡。 展开更多
关键词 视网膜müller细胞 微小RNA-26a-5p(miR-26a-5p) PTEN/PI3K/Akt 炎症 糖尿病视网膜病变
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视网膜再生中调控Müller细胞重编程的表观遗传修饰和微环境因素研究进展
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作者 廖怿 何婉玲 《厦门大学学报(自然科学版)》 CAS CSCD 北大核心 2024年第5期850-866,共17页
[背景]Müller细胞(Müller glia,MG)重编程是视网膜再生领域的研究热点.与斑马鱼(Danio rerio)不同,哺乳动物视网膜损伤后MG丧失再生视网膜能力,发生反应性胶质化产生胶质瘢痕,导致哺乳动物MG重编程再生视网膜能力丧失的分子... [背景]Müller细胞(Müller glia,MG)重编程是视网膜再生领域的研究热点.与斑马鱼(Danio rerio)不同,哺乳动物视网膜损伤后MG丧失再生视网膜能力,发生反应性胶质化产生胶质瘢痕,导致哺乳动物MG重编程再生视网膜能力丧失的分子机制仍存在许多不清楚之处.[进展]随着干细胞理论和研究方法的不断进步,越来越多研究利用单细胞测序等技术从转录、表观遗传修饰、细胞外微环境等多层次深入挖掘视网膜再生中MG重编程的调控机制,以期实现哺乳动物的视网膜再生.本文总结了不同物种中已发现的影响MG重编程能力差异的关键分子,着重关注表观遗传修饰和微环境因素.[展望]视网膜再生中MG重编程是受细胞内外多种因素协同调控的复杂过程.对斑马鱼和哺乳动物视网膜再生中MG重编程影响因素进行详细的对比分析,将有助于突破哺乳动物视网膜再生瓶颈,为开发有临床转化潜力的疗法提供新的途径. 展开更多
关键词 müller细胞 视网膜再生 表观遗传修饰 微环境
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Müller细胞在常见眼底疾病中的研究进展
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作者 王金燕 刘春梦 +2 位作者 郭星雨 韩暄 叶河江 《中医眼耳鼻喉杂志》 2024年第3期156-158,共3页
神经胶质细胞在维持中枢神经系统稳态方面发挥关键作用,Müller细胞作为视网膜中主要神经胶质细胞,在维持视网膜结构和功能正常方面有重要作用。Müller细胞的损伤会导致视网膜功能障碍。近年来许多研究表明视网膜功能是否正常... 神经胶质细胞在维持中枢神经系统稳态方面发挥关键作用,Müller细胞作为视网膜中主要神经胶质细胞,在维持视网膜结构和功能正常方面有重要作用。Müller细胞的损伤会导致视网膜功能障碍。近年来许多研究表明视网膜功能是否正常很大程度上取决于Müller细胞。本文综述了近五年来Müller细胞在常见的眼底疾病中的作用及相关机制,以期深入了解Müller细胞在常见的眼底疾病中的影响与价值,为眼底疾病发病机制的研究、筛查、诊断、及预防提供新思路。 展开更多
关键词 müller细胞 糖尿病视网膜病变 青光眼 早产儿视网膜病变
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Impaired pericyte-Müller glia interaction via PDGFRβ suppression aggravates photoreceptor loss in a rodent model of light-induced retinal injury
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作者 Wei Xu Li-Jin Cui +3 位作者 Xiao-Ying Yang Xiao-Yuan Cui Jian Guo Guo-Xing Xu 《International Journal of Ophthalmology(English edition)》 SCIE CAS 2024年第10期1800-1808,共9页
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 r... 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. 展开更多
关键词 PERICYTE müller glia light-induced retinal injury platelet-derived growth factor receptorβ signal pathway
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Investigating Müller glia reprogramming in mice: a retrospective of the last decade, and a look to the future
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作者 Zhiyuan Yin Jiahui Kang +3 位作者 Xuan Cheng Hui Gao Shujia Huo Haiwei Xu 《Neural Regeneration Research》 SCIE CAS 2025年第4期946-959,共14页
Müller glia,as prominent glial cells within the retina,plays a significant role in maintaining retinal homeostasis in both healthy and diseased states.In lower vertebrates like zebrafish,these cells assume respon... Müller glia,as prominent glial cells within the retina,plays a significant role in maintaining retinal homeostasis in both healthy and diseased states.In lower vertebrates like zebrafish,these cells assume responsibility for spontaneous retinal regeneration,wherein endogenous Müller glia undergo proliferation,transform into Müller glia-derived progenitor cells,and subsequently regenerate the entire retina with restored functionality.Conversely,Müller glia in the mouse and human retina exhibit limited neural reprogramming.Müller glia reprogramming is thus a promising strategy for treating neurodegenerative ocular disorders.Müller glia reprogramming in mice has been accomplished with remarkable success,through various technologies.Advancements in molecular,genetic,epigenetic,morphological,and physiological evaluations have made it easier to document and investigate the Müller glia programming process in mice.Nevertheless,there remain issues that hinder improving reprogramming efficiency and maturity.Thus,understanding the reprogramming mechanism is crucial toward exploring factors that will improve Müller glia reprogramming efficiency,and for developing novel Müller glia reprogramming strategies.This review describes recent progress in relatively successful Müller glia reprogramming strategies.It also provides a basis for developing new Müller glia reprogramming strategies in mice,including epigenetic remodeling,metabolic modulation,immune regulation,chemical small-molecules regulation,extracellular matrix remodeling,and cell-cell fusion,to achieve Müller glia reprogramming in mice. 展开更多
关键词 cell fusion chemical small-molecules EPIGENETIC extracellular matrix immune metabolic mICE müller glia neurodegenerative diseases REPROGRAmmING retina regeneration
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Müller细胞胶质间质转化在视网膜纤维化疾病中的作用
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作者 王乾坤 索龙 刘爽 《国际眼科杂志》 CAS 2024年第11期1747-1752,共6页
胶质细胞间质转化(GMT)指胶质细胞在各种因素刺激下逐渐获得间质细胞表型和特征的生物学过程,与视网膜纤维化疾病密切相关。Müller细胞是视网膜上最主要的大胶质细胞,在受到各种病理因素刺激时被激活并发生转分化。目前,已有研究表... 胶质细胞间质转化(GMT)指胶质细胞在各种因素刺激下逐渐获得间质细胞表型和特征的生物学过程,与视网膜纤维化疾病密切相关。Müller细胞是视网膜上最主要的大胶质细胞,在受到各种病理因素刺激时被激活并发生转分化。目前,已有研究表明,Müller细胞GMT与糖尿病视网膜病变、特发性黄斑前膜(iERM)、年龄相关性黄斑变性(ARMD)、增生性玻璃体视网膜病变(PVR)等多种疾病密切相关。尽管GMT相关调控机制尚不完全明确,但其作为一个潜在的干预靶点,具有良好的研究前景。了解Müller细胞GMT在视网膜疾病中的研究进展,能够为多种视网膜疾病的早期诊断和治疗提供新思路,对于全面揭示细胞转型家族在视网膜疾病中的交互作用具有重要的临床和科学意义。 展开更多
关键词 müller细胞 胶质间质转化 视网膜纤维化
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Müller cells are activated in response to retinal outer nuclear layer degeneration in rats subjected to simulated weightlessness conditions
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作者 Yuxue Mu Ning Zhang +7 位作者 Dongyu Wei Guoqing Yang Lilingxuan Yao Xinyue Xu Yang Li Junhui Xue Zuoming Zhang Tao Chen 《Neural Regeneration Research》 SCIE CAS 2025年第7期2116-2128,共13页
A microgravity environment has been shown to cause ocular damage and affect visual acuity,but the underlying mechanisms remain unclear.Therefore,we established an animal model of weightlessness via tail suspension to ... A microgravity environment has been shown to cause ocular damage and affect visual acuity,but the underlying mechanisms remain unclear.Therefore,we established an animal model of weightlessness via tail suspension to examine the pathological changes and molecular mechanisms of retinal damage under microgravity.After 4 weeks of tail suspension,there were no notable alterations in retinal function and morphology,while after 8 weeks of tail suspension,significant reductions in retinal function were observed,and the outer nuclear layer was thinner,with abundant apoptotic cells.To investigate the mechanism underlying the degenerative changes that occurred in the outer nuclear layer of the retina,proteomics was used to analyze differentially expressed proteins in rat retinas after 8 weeks of tail suspension.The results showed that the expression levels of fibroblast growth factor 2(also known as basic fibroblast growth factor)and glial fibrillary acidic protein,which are closely related to Müller cell activation,were significantly upregulated.In addition,Müller cell regeneration and Müller cell gliosis were observed after 4 and 8 weeks,respectively,of simulated weightlessness.These findings indicate that Müller cells play an important regulatory role in retinal outer nuclear layer degeneration during weightlessness. 展开更多
关键词 glial fibrous acidic protein GLIOSIS müller cells nerve growth factor neural differentiation neurodegeneration proteomic retinal degeneration retinal outer nuclear layer simulated weightlessness
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股骨远端前外侧切口锁定钢板、前侧附加重建钢板在股骨远端Müller分型C2、C3型骨折治疗中的应用分析
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作者 仲彪 吕书军 史少华 《临床和实验医学杂志》 2024年第8期841-845,共5页
目的 探究股骨远端前外侧切口锁定钢板、前侧附加重建钢板在股骨远端Müller分型C2、C3型骨折治疗中的应用效果。方法 回顾性选取2018年3月至2022年6月在海安市人民医院接受治疗的120例股骨远端Müller分型C2、C3型骨折患者作... 目的 探究股骨远端前外侧切口锁定钢板、前侧附加重建钢板在股骨远端Müller分型C2、C3型骨折治疗中的应用效果。方法 回顾性选取2018年3月至2022年6月在海安市人民医院接受治疗的120例股骨远端Müller分型C2、C3型骨折患者作为本研究的研究对象,按照治疗方法不同分为对照组和研究组,每组各60例。对照组患者接受前外侧切口锁定钢板治疗,研究组患者接受前外侧切口锁定钢板+前侧附加重建钢板治疗。门诊随访12个月,比较两组患者临床指标(手术时间、术中出血量、术中C型壁透视次数、术后下地康复时间、骨折愈合时间及骨折愈合率),治疗效果,膝关节功能,术后1、2、3、6个月的膝关节活动度,术后6个月患者的下肢最大伸膝肌力矩、最大内屈角及术后并发症发生情况。结果 两组手术时间、术中出血量、术中C型壁透视次数及骨折愈合率比较,差异均无统计学意义(P>0.05);研究组术后下地康复时间、骨折愈合时间分别为(4.89±0.98)周、(6.61±1.06)个月,均短于对照组[(6.04±1.55)周、(8.45±1.02)个月],差异均有统计学意义(P<0.05)。研究组的治疗优良率为91.67%,高于对照组(78.33%),差异有统计学意义(P<0.05)。术后6个月,两组膝关节功能比较,差异无统计学意义(P>0.05)。术后1、2个月,两组膝关节活动度比较,差异均无统计学意义(P>0.05);术后3、6个月,研究组患者的膝关节活动度分别为(103.56±2.38)°、(115.68±2.77)°,均高于对照组[(92.45±5.46)°、(95.88±3.49)°],差异均有统计学意义(P<0.05)。术后6个月,研究组在触底即时及支撑末期时最大伸膝肌力矩分别为(22.66±1.26)、(18.99±2.15) Nm,均高于对照组[(19.56±2.01)、(17.58±1.87) Nm],最大内屈角分别为(3.56±0.26)°、(6.55±0.51)°,均小于对照组[(4.55±0.31)°、(7.66±0.46)°],差异均有统计学意义(P<0.05)。两组随访期内并发症发生率比较,差异无统计学意义(P>0.05)。结论 使用前侧附加重建钢板治疗股骨远端Müller分型C2、C3型骨折,相比前外侧切口锁定钢板治疗,能够提高治疗的优良率,缩短术后下地康复时间和骨折愈合时间,改善远期膝关节活动度、最大伸膝肌力矩和最大内屈角。 展开更多
关键词 股骨骨折 前外侧切口锁定钢板 前侧附加重建钢板 müller分型
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基于NF-κB/NLRP3通路的芍药苷对缺氧诱导视网膜Müller细胞的影响 被引量:2
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作者 孔令春 邹红 +3 位作者 李景景 杨宇琴 唐慧新 缪晚虹 《中国中医药信息杂志》 CAS CSCD 2023年第2期106-111,共6页
目的观察芍药苷对缺氧诱导视网膜Müller细胞的保护作用,探讨其作用机制。方法将rMC-1细胞分为对照组、模型组和芍药苷高、低浓度组,以1200、600μmol/L芍药苷干预缺氧条件下的rMC-1细胞,CCK8检测细胞活力,ELISA检测上清液血管内皮... 目的观察芍药苷对缺氧诱导视网膜Müller细胞的保护作用,探讨其作用机制。方法将rMC-1细胞分为对照组、模型组和芍药苷高、低浓度组,以1200、600μmol/L芍药苷干预缺氧条件下的rMC-1细胞,CCK8检测细胞活力,ELISA检测上清液血管内皮生长因子(VEGF)、白细胞介素(IL)-1β含量,Western blot检测细胞核因子(NF)-κB p65、NLRP3、凋亡相关斑点样蛋白(ASC)、半胱氨酸蛋白酶-1前体(pro-Caspase-1)蛋白表达,RT-PCR检测IL-1β、VEGF、NF-κB、NLRP3、ASC、Caspase-1基因表达。结果与对照组比较,模型组rMC-1细胞活力显著降低,上清液VEGF、IL-1β含量显著增加,细胞NF-κB p65、NLRP3、ASC、pro-Caspase-1蛋白表达显著升高,IL-1β、VEGF、NF-κB、NLRP3、ASC、Caspase-1基因表达显著升高,差异均有统计学意义(P<0.05,P<0.01,P<0.001);与模型组比较,芍药苷高、低浓度组rMC-1细胞活力显著升高,上清液VEGF、IL-1β含量显著减少,芍药苷高浓度组细胞NF-κB p65、NLRP3、ASC、pro-Caspase-1蛋白表达显著降低,IL-1β、VEGF、NF-κB、NLRP3、ASC、Caspase-1基因表达显著降低,差异均有统计学意义(P<0.05,P<0.01,P<0.001)。结论芍药苷可促进视网膜Müller细胞rMC-1增殖,抑制缺氧诱导的VEGF和IL-1β分泌,其机制可能与抑制NF-κB/NLRP3通路有关。 展开更多
关键词 芍药苷 视网膜缺氧 müller细胞 NLRP3炎症小体 血管内皮生长因子 白细胞介素-1Β
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加味桃红四物汤对视网膜Müller细胞缺氧损伤的保护作用 被引量:3
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作者 孔令春 邹红 +2 位作者 李景景 凌芸 唐慧新 《国际眼科杂志》 CAS 北大核心 2023年第1期17-22,共6页
目的:探讨加味桃红四物汤(MTSD)对视网膜Müller细胞rMC-1缺氧损伤的保护作用。方法:用加味桃红四物汤含药血清干预缺氧条件下rMC-1细胞,随机分为正常对照组(21%O_(2))、缺氧模型组(1%O_(2))、含药血清低(1%O_(2)+5%含药血清)、中(1... 目的:探讨加味桃红四物汤(MTSD)对视网膜Müller细胞rMC-1缺氧损伤的保护作用。方法:用加味桃红四物汤含药血清干预缺氧条件下rMC-1细胞,随机分为正常对照组(21%O_(2))、缺氧模型组(1%O_(2))、含药血清低(1%O_(2)+5%含药血清)、中(1%O_(2)+10%含药血清)、高剂量组(1%O_(2)+15%含药血清),CCK-8法检测细胞的活力,ELISA法检测血管内皮生长因子(VEGF)和色素上皮衍生因子(PEDF)分泌,Western blot检测磷酸化转录激活因子3(p-STAT3)、转录激活因子3(STAT3)和缺氧诱导因子-1α(HIF-1α)的蛋白表达,Real time PCR检测VEGF、PEDF、STAT3和HIF-1α的基因表达。结果:在1%O_(2)条件下培养48h,rMC-1细胞活力较正常对照组明显受到抑制(P<0.05),加味桃红四物汤含药血清低、中剂量组均可以改善rMC-1细胞缺氧48h的细胞存活率(P<0.05),而高剂量组无改善作用(P>0.05)。加味桃红四物汤含药血清低、中剂量组均可减少缺氧条件下rMC-1细胞上清液VEGF的蛋白表达量(P<0.05),但不能增加PEDF的蛋白含量(P>0.05),对p-STAT3和HIF-1α在蛋白水平均有下调作用(P<0.05),且低剂量组抑制作用优于中剂量(P<0.05)。加味桃红四物汤含药血清中剂量组对缺氧后rMC-1细胞STAT3的蛋白表达有上调作用(P<0.05)。加味桃红四物汤含药血清低、中剂量组对缺氧后rMC-1细胞VEGF基因表达均有下调作用(P<0.05),对PEDF基因表达均有上调作用(P<0.05),且低剂量组优于中剂量(P<0.05);并且加味桃红四物汤含药血清低剂量可下调缺氧后STAT3和HIF-1α的基因表达(P<0.05)。结论:加味桃红四物汤含药血清可能通过抑制STAT3/HIF-1α通路,下调缺氧诱导的视网膜Müller细胞rMC-1的VEGF蛋白和基因表达,上调PEDF基因表达,减轻该细胞的缺氧损伤。 展开更多
关键词 加味桃红四物汤 视网膜缺氧 müller细胞 血管内皮生长因子 色素上皮衍生因子 缺氧诱导因子-1Α
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视网膜Müller细胞重编程研究进展
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作者 张小丽 张书强 徐绘 《解剖学报》 CAS CSCD 北大核心 2023年第4期484-489,共6页
视网膜退行性疾病导致的失明严重影响人类健康。哺乳动物视网膜损伤后无法自我修复,而斑马鱼的视网膜具有较强的再生能力,能再生所有类型的视网膜神经元并恢复视觉。斑马鱼的视网膜再生依赖于一种神经胶质细胞——Müller细胞。斑... 视网膜退行性疾病导致的失明严重影响人类健康。哺乳动物视网膜损伤后无法自我修复,而斑马鱼的视网膜具有较强的再生能力,能再生所有类型的视网膜神经元并恢复视觉。斑马鱼的视网膜再生依赖于一种神经胶质细胞——Müller细胞。斑马鱼视网膜损伤后Müller细胞重编程并增殖产生祖细胞,后者进一步分化为新生的视网膜神经元。近年来,基于Müller细胞的视网膜再生研究取得了许多重要进展。我们就斑马鱼视网膜再生的机制和哺乳动物Müller细胞重编程的研究进展做一综述。 展开更多
关键词 视网膜 再生 重编程 müller细胞 斑马鱼
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Trim9调控视网膜Müller细胞向神经节细胞定向分化 被引量:1
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作者 李金香 曾琦 《中南大学学报(医学版)》 CAS CSCD 北大核心 2023年第10期1561-1571,共11页
目的:青光眼是不可逆性致盲性眼病的主要病因,目前尚无有效疗法逆转青光眼的视觉系统损害。最近发现干细胞疗法有望使受损的视网膜神经元修复和再生,但是在干细胞来源方面仍然存在较大挑战。本研究探寻一种将视网膜Müller细胞去分... 目的:青光眼是不可逆性致盲性眼病的主要病因,目前尚无有效疗法逆转青光眼的视觉系统损害。最近发现干细胞疗法有望使受损的视网膜神经元修复和再生,但是在干细胞来源方面仍然存在较大挑战。本研究探寻一种将视网膜Müller细胞去分化为视网膜干细胞,进一步高效定向分化为视网膜神经节细胞的方案,以期为青光眼的干细胞治疗提供新的细胞获取途径。方法:用表皮细胞生长因子和成纤维细胞生长因子2诱导大鼠视网膜Müller细胞去分化为视网膜干细胞。构建Trim9过表达慢病毒(PGC-FU-Trim9-GFP),感染由Müller细胞诱导去分化而来的视网膜干细胞,通过荧光显微镜观察和流式细胞术评估病毒感染效率。用视黄酸和脑源性神经营养因子处理过表达或未过表达Trim9的视网膜干细胞以诱导其分化为神经元和神经胶质细胞。采用免疫荧光、PCR/real-time RT-PCR和蛋白质印迹法检测各细胞标志物(GLAST、GS、rhodopsin、PKC、HPC-1、Calbindin、Thy1.1、Brn-3b、Nestin、Pax6)的表达。结果:表皮细胞生长因子和成纤维细胞生长因子2处理后的大鼠视网膜Müller细胞表达视网膜干细胞标志物Nestin和Pax6。视黄酸和脑源性神经营养因子处理后的过表达Trim9的视网膜干细胞Thy1.1阳性细胞明显增多,表明其定向分化为视网膜神经节细胞。结论:本研究成功将大鼠视网膜Müller细胞去分化为视网膜干细胞,并发现Trim9可有效促进由视网膜Müller细胞去分化而来的视网膜干细胞定向分化为视网膜神经节细胞。 展开更多
关键词 青光眼 müller细胞 Trim9 视网膜干细胞 视网膜神经节细胞
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Soxllb regulates the migration and fate determination of Müller glia-derived progenitors during retina regeneration in zebrafish 被引量:4
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作者 Kaida Song Zihao Lin +5 位作者 Lining Cao Bowen Lu Yuxi Chen Shuqiang Zhang Jianfeng Lu Hui Xu 《Neural Regeneration Research》 SCIE CAS CSCD 2023年第2期445-450,共6页
The transcription factor Sox11 plays important roles in retinal neurogenesis during vertebrate eye development.However,its function in retina regeneration remains elusive.Here we report that Sox11 b,a zebrafish Sox11 ... The transcription factor Sox11 plays important roles in retinal neurogenesis during vertebrate eye development.However,its function in retina regeneration remains elusive.Here we report that Sox11 b,a zebrafish Sox11 homolog,regulates the migration and fate determination of Müller glia-derived progenitors(MGPCs)in an adult zebrafish model of mechanical retinal injury.Following a stab injury,the expression of Sox11 b was induced in proliferating MGPCs in the retina.Sox11 b knockdown did not affect MGPC formation at 4 days post-injury,although the nuclear morphology and subsequent radial migration of MGPCs were alte red.At 7 days post-injury,Sox11 b knockdown res ulted in an increased proportion of MGPCs in the inner retina and a decreased propo rtion of MGPCs in the outer nuclear layer,compared with controls.Furthermore,Sox11 b knockdown led to reduced photoreceptor regeneration,while it increased the numbe rs of newborn amacrines and retinal ganglion cells.Finally,quantitative polymerase chain reaction analysis revealed that Sox11 b regulated the expression of Notch signaling components in the retina,and Notch inhibition partially recapitulated the Sox11 b knockdown phenotype,indicating that Notch signaling functions downstream of Sox11 b.Our findings imply that Sox11 b plays key roles in MGPC migration and fate determination during retina regeneration in zebrafish,which may have critical im plications for future explorations of retinal repair in mammals. 展开更多
关键词 cell migration fate determination müllerglia müller glia-derived progenitor Notch signaling photoreceptor retina regeneration Sox11 transcription factor ZEBRAFISH
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Overexpressing NeuroD1 reprograms Müller cells into various types of retinal neurons 被引量:5
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作者 Di Xu Li-Ting Zhong +6 位作者 Hai-Yang Cheng Zeng-Qiang Wang Xiong-Min Chen Ai-Ying Feng Wei-Yi Chen Gong Chen Ying Xu 《Neural Regeneration Research》 SCIE CAS CSCD 2023年第5期1124-1131,共8页
The onset of retinal degenerative disease is often associated with neuronal loss. Therefore, how to regenerate new neurons to restore vision is an important issue. NeuroD1 is a neural transcription factor with the abi... The onset of retinal degenerative disease is often associated with neuronal loss. Therefore, how to regenerate new neurons to restore vision is an important issue. NeuroD1 is a neural transcription factor with the ability to reprogram brain astrocytes into neurons in vivo. Here, we demonstrate that in adult mice, NeuroD1 can reprogram Müller cells, the principal glial cell type in the retina, to become retinal neurons. Most strikingly, ectopic expression of NeuroD1 using two different viral vectors converted Müller cells into different cell types. Specifically, AAV7 m8 GFAP681::GFP-ND1 converted Müller cells into inner retinal neurons, including amacrine cells and ganglion cells. In contrast, AAV9 GFAP104::ND1-GFP converted Müller cells into outer retinal neurons such as photoreceptors and horizontal cells, with higher conversion efficiency. Furthermore, we demonstrate that Müller cell conversion induced by AAV9 GFAP104::ND1-GFP displayed clear dose-and time-dependence. These results indicate that Müller cells in adult mice are highly plastic and can be reprogrammed into various subtypes of retinal neurons. 展开更多
关键词 amacrine cell ganglion cell horizontal cell in vivo reprogramming müller cell NeuroD1 PHOTORECEPTOR REGENERATION RETINA retinal degeneration
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Neural and Müller glial adaptation of the retina to photoreceptor degeneration 被引量:2
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作者 Henri O.Leinonen Edward Bull Zhongjie Fu 《Neural Regeneration Research》 SCIE CAS CSCD 2023年第4期701-707,共7页
The majority of inherited retinal degenerative diseases and dry age-related macular degeneration are characterized by decay of the outer retina and photoreceptors,which leads to progressive loss of vision.The inner re... The majority of inherited retinal degenerative diseases and dry age-related macular degeneration are characterized by decay of the outer retina and photoreceptors,which leads to progressive loss of vision.The inner retina,including second-and third-order retinal neurons,also shows aberrant structural changes at all stages of degeneration.Müller glia,the major glial cells maintain retinal homeostasis,activating and rearranging immediately in response to photoreceptor stress.These phenomena are collectively known as retinal remodeling and are anatomically well described,but their impact on visual function is less well characterized.Retinal remodeling has traditionally been considered a detrimental chain of events that decreases visual function.However,emerging evidence from functional assays suggests that remodeling could also be a part of a survival mechanism wherein the inner retina responds plastically to outer retinal degeneration.The visual system’s first synapses between the photoreceptors and bipolar cells undergo rewiring and functionally compensate to maintain normal signal output to the brain.Distinct classes of retinal ganglion cells remain even after the massive loss of photoreceptors.Müller glia possess the regenerative potential for retinal recovery and possibly exert adaptive transcriptional changes in response to neuronal loss.These types of homeostatic changes could potentially explain the well-maintained visual function observed in patients with inherited retinal degenerative diseases who display prominent anatomic retinal pathology.This review will focus on our current understanding of retinal neuronal and Müller glial adaptation for the potential preservation of retinal activity during photoreceptor degeneration.Targeting retinal self-compensatory responses could help generate universal strategies to delay sensory disease progression. 展开更多
关键词 bipolar cells ELECTRORETINOGRAPHY müller glia PHOTORECEPTORS plasticity retinal degeneration retinal neuron retinal remodeling retinal ganglion cells
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艳山姜挥发油调控CaMKⅡ信号改善糖尿病诱导视网膜Müller细胞自噬障碍
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作者 陈冰 杨红 +6 位作者 杨惠 陈永鑫 甘诗泉 文波 蒋朝晖 沈祥春 李悦 《中南药学》 2023年第10期2616-2621,共6页
目的探讨艳山姜挥发油(EOFAZ)对糖尿病诱导视网膜Müller细胞功能障碍的保护作用及机制。方法视网膜Müller细胞使用不同剂量的EOFAZ进行预处理1 h后,采用高糖(30 mmol·L^(-1))孵育48 h,Western blot法检测细胞中自噬信号B... 目的探讨艳山姜挥发油(EOFAZ)对糖尿病诱导视网膜Müller细胞功能障碍的保护作用及机制。方法视网膜Müller细胞使用不同剂量的EOFAZ进行预处理1 h后,采用高糖(30 mmol·L^(-1))孵育48 h,Western blot法检测细胞中自噬信号Beclin1、LC3Ⅱ/Ⅰ、P62蛋白的表达水平;qRT-PCR分析细胞中P62 mRNA、Beclin1 mRNA的转录水平,免疫荧光实验分析LC3Ⅱ/Ⅰ、P62的表达。并进一步使用钙离子螯合剂BAPTA-AM及CaMKⅡ特异性抑制剂KN93孵育细胞,检测自噬信号LC3Ⅱ/Ⅰ、Beclin1、P62蛋白表达水平。使用自噬抑制剂氯喹(CQ)孵育细胞,检测细胞中CaMKⅡ及自噬信号LC3Ⅱ/Ⅰ、P62蛋白的表达。结果与高糖组相比,EOFAZ可明显上调Beclin1、LC3Ⅱ/Ⅰ、P62的表达水平;使用BAPTA-AM及KN93孵育细胞与EOFAZ的作用类似。同时观察到EOFAZ与BAPTA-AM或KN93联合应用后,与EOFAZ单独作用的结果无明显差异。当EOFAZ与CQ共同孵育细胞后,EOFAZ对自噬相关蛋白下调的改善作用可被抑制,对CaMKⅡ的磷酸化水平无明显影响。结论EOFAZ对高糖诱导的视网膜Müller细胞自噬障碍具有明显的改善作用,其作用可能是通过抑制CaMKⅡ信号发挥的。 展开更多
关键词 艳山姜挥发油 糖尿病 视网膜müller细胞 自噬障碍 CamKⅡ
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神经胶质成熟因子-β诱导糖尿病大鼠视网膜Müller细胞炎症反应的机制研究 被引量:2
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作者 罗影 单伟 张俏 《天津医药》 CAS 北大核心 2023年第4期387-391,共5页
目的 研究神经胶质成熟因子-β(GMFB)对糖尿病大鼠视网膜Müller细胞活化的作用及相关机制。方法SPF级雄性SD大鼠60只,采用腹腔注射链脲佐菌素(STZ,55 mg/kg)制备糖尿病模型后分为STZ组、STZ+AAVGMFB组和STZ+AAV-GMFB+K252a组,每组1... 目的 研究神经胶质成熟因子-β(GMFB)对糖尿病大鼠视网膜Müller细胞活化的作用及相关机制。方法SPF级雄性SD大鼠60只,采用腹腔注射链脲佐菌素(STZ,55 mg/kg)制备糖尿病模型后分为STZ组、STZ+AAVGMFB组和STZ+AAV-GMFB+K252a组,每组15只。另取15只正常大鼠作为CON组。STZ+AAV-GMFB组和STZ+AAV-GMFB+K252a组大鼠于成模8周后玻璃体腔单次注射AAV-GMFB腺病毒载体5μL。STZ+AAV-GMFB+K252a组在注射腺病毒基础上给予腹腔注射25μg/(kg·d)的K252a。12周后,免疫荧光检测GMFB在Müller细胞中的表达,免疫组织化学染色检测视网膜胶质纤维酸性蛋白(GFAP)的表达,酶联免疫吸附试验检测视网膜炎性因子肿瘤坏死因子-α(TNF-α)、白细胞介素(IL)-1β、IL-6的表达,Western blot检测GMFB、脑源性神经营养因子(BDNF)及磷酸化酪氨酸激酶受体B(p-TrkB)蛋白相对表达水平。HE染色检测视网膜病理改变。结果 GMFB在Müller细胞中大量表达。与CON组比较,STZ组GMFB、GFAP表达及TNF-α、IL-1β、IL-6水平增加,BDNF、p-TrkB蛋白表达减少,视网膜神经节细胞(RGC)排列紊乱,数量减少;与STZ组比较,STZ+AAV-GMFB组GMFB、GFAP表达及TNF-α、IL-1β、IL-6水平降低,BDNF、p-TrkB蛋白表达增加,RGC排列整齐,数量增加。TrkB抑制剂K252a能大部分逆转AAVGMFB的保护作用。结论 糖尿病大鼠视网膜GMFB表达增加,诱导了Müller细胞活化,加重了炎症反应,该作用与抑制BDNF/TrkB信号通路有关。 展开更多
关键词 糖尿病 糖尿病视网膜病变 炎症 神经胶质成熟因子-β müller细胞 BDNF/TrkB信号通路
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脂多糖对小鼠视网膜Müller细胞和小胶质细胞共培养体系中炎症因子水平的影响及其机制 被引量:1
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作者 胡志宽 何思琦 +3 位作者 蒋维杰 赵贵芳 张佳 齐玲 《吉林大学学报(医学版)》 CAS CSCD 北大核心 2023年第5期1140-1146,共7页
目的:观察脂多糖(LPS)诱导小鼠视网膜单独培养Müller细胞和Müller细胞与小胶质细胞共培养2种体系中的炎症反应,阐明Müller细胞与小胶质细胞的相互作用机制。方法:培养Müller细胞QMMuC-1和小胶质细胞BV2,免疫荧光染... 目的:观察脂多糖(LPS)诱导小鼠视网膜单独培养Müller细胞和Müller细胞与小胶质细胞共培养2种体系中的炎症反应,阐明Müller细胞与小胶质细胞的相互作用机制。方法:培养Müller细胞QMMuC-1和小胶质细胞BV2,免疫荧光染色方法观察2种细胞形态表现。实验分为单独培养对照组[QMMuC-1细胞单独培养,采用磷酸盐(PBS)缓冲液处理]、共培养对照组(QMMuC-1细胞和BV2细胞共培养,细胞比例1∶1,采用PBS缓冲液处理)、单独培养实验组(QMMuC-1细胞单独培养,采用10 mg·L^(-1)LPS处理)和共培养实验组(QMMuC-1细胞和BV2细胞共培养,采用10 mg·L^(-1)LPS处理)。采用免疫荧光染色法观察各组细胞中胶质纤维酸性蛋白(GFAP)水平,实时荧光定量PCR(RT-qPCR)法检测各组QMMuC-1细胞中白细胞介素1β(IL-1β)、白细胞介素6(IL-6)和肿瘤坏死因子α(TNF-α)mRNA表达水平。结果:QMMuC-1细胞中神经胶质细胞标志物谷氨酰胺合成酶(GS)和GFAP阳性,BV2细胞中小胶质细胞标志物离子钙接头蛋白分子1(Iba-1)阳性。与单独培养对照组比较,单独培养实验组QMMuC-1细胞中GFAP水平升高1.7倍(P=0.005);与共培养对照组比较,共培养实验组QMMuC-1细胞中GFAP水平升高2倍(P=0.003),细胞形态逐渐变成梭形;与单独培养实验组比较,共培养实验组QMMuC-1细胞中GFAP水平升高1.4倍(P=0.0006),大部分细胞呈梭形。与单独培养对照组比较,单独培养实验组QMMuC-1细胞中IL-1β、IL-6和TNF-αmRNA表达水平升高,但差异无统计学意义(P>0.05);与共培养对照组比较,共培养实验组QMMuC-1细胞中IL-1β、IL-6和TNF-αmRNA表达水平升高(P<0.05);与单独培养实验组比较,共培养实验组QMMuC-1细胞中IL-1β和TNF-αmRNA表达水平升高(P<0.05)。结论:LPS可能通过诱导小胶质细胞激活后释放炎症因子作用于Müller细胞,并加剧了Müller细胞的炎症反应。 展开更多
关键词 müller细胞 小胶质细胞 共培养 脂多糖 炎症反应
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改良提上睑肌延长术联合Müller肌切除术治疗上睑退缩的疗效观察 被引量:1
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作者 方涛 杨宏刚 +1 位作者 张承武 胡金 《中国美容医学》 CAS 2023年第1期15-18,共4页
目的:探讨改良提上睑肌延长术联合Müller肌切除术治疗上睑退缩的疗效。方法:选取2017年10月-2020年10月在笔者医院就诊的上睑退缩患者59例。对所有患者实施改良提上睑肌延长术联合Müller肌切除术。术后6个月,记录临床效果、... 目的:探讨改良提上睑肌延长术联合Müller肌切除术治疗上睑退缩的疗效。方法:选取2017年10月-2020年10月在笔者医院就诊的上睑退缩患者59例。对所有患者实施改良提上睑肌延长术联合Müller肌切除术。术后6个月,记录临床效果、眼睑及眼表指标、并发症和生活质量情况。结果:术后6个月,59例上睑退缩患者中,完全矫正42例(71.19%),改善16例(27.12%),无效1例(1.69%),总有效率为98.31%(58/59)。术后,患者睑裂高度、上方巩膜露白均低于术前,上睑覆盖角膜高度高于术前,差异有统计学意义(P<0.05);术前术后患者上睑肌力比较,差异无统计学意义(P>0.05)。术后,患者泪膜破裂时间、泪液基础分泌试验长度均优于术前,差异有统计学意义(P<0.05)。59例上睑退缩患者中,4例患者有不同程度的眼睑肿胀,患者均无感染、血肿、颞侧巩膜暴露、复发等并发症。术后,患者生活质量评分均高于术前,差异有统计学意义(P<0.05)。结论:改良提上睑肌延长术联合Müller肌切除术在上睑退缩治疗中疗效确切,能减轻临床症状,改善患者生活质量,且并发症少。 展开更多
关键词 上睑退缩 改良提上睑肌延长术 müller肌切除术 并发症 生活质量
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P-aminobenzoic acid promotes retinal regeneration through activation of Ascl1a in zebrafish 被引量:1
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作者 Meihui He Mingfang Xia +3 位作者 Qian Yang Xingyi Chen Haibo Li Xiaobo Xia 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第8期1849-1856,共8页
The retina of zebrafish can regenerate completely after injury.M ultiple studies have demonstrated that metabolic alte rations occur during retinal damage;however to date no study has identified a link between metabol... The retina of zebrafish can regenerate completely after injury.M ultiple studies have demonstrated that metabolic alte rations occur during retinal damage;however to date no study has identified a link between metabolites and retinal regeneration of zebrafish.Here,we performed an unbiased metabolome sequencing in the N-methyl-D-aspartic acid-damaged retinas of zebrafish to demonstrate the metabolomic mechanism of retinal regeneration.Among the differentially-ex pressed metabolites,we found a significant decrease in p-aminobenzoic acid in the N-methyl-D-aspartic acid-damaged retinas of zebrafish.Then,we investigated the role of p-aminobenzoic acid in retinal regeneration in adult zebrafish.Impo rtantly,p-aminobenzoic acid activated Achaetescute complex-like 1a expression,thereby promoting Müller glia reprogramming and division,as well as Müller glia-derived progenitor cell proliferation.Finally,we eliminated folic acid and inflammation as downstream effectors of PABA and demonstrated that PABA had little effect on Müller glia distribution.Taken together,these findings show that PABA contributes to retinal regeneration through activation of Achaetescute complex-like 1a expression in the N-methyl-Daspartic acid-damaged retinas of zebrafish. 展开更多
关键词 Achaetescute complex-like 1a(Ascl1a) metabolomics müller glia p-aminobenzoic acid(PABA) RETINA REGENERATION ZEBRAFISH
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