Invest Ophthalmol Vis Sci:视网膜分支静脉阻塞时小胶质细胞的活化与循环巨噬细胞的募集

2017-03-31 luowenbo MedSci原创

该研究目的在于探索试验性视网膜分支静脉阻塞(BRVO)时视网膜小胶质细胞的活化与巨噬细胞募集的特征。

视网膜分支静脉阻塞时小胶质细胞的活化与循环巨噬细胞的募集

该研究目的在于探索试验性视网膜分支静脉阻塞(BRVO)时视网膜小胶质细胞的活化与巨噬细胞募集的特征。

利用BALB/c小鼠建立BRVO模型,并研究其组化改变。采用哌莫硝唑盐酸法显示组织缺氧改变,采用组织学和流式细胞术定量检测单核细胞来源的视网膜细胞。将Cx3cr1(gfp/gfp)小鼠的骨髓移植到致死剂量辐射过的野生型小鼠(BALB/c小鼠),从而形成嵌合体小鼠,用嵌合体小鼠模型探讨侵袭性血源性巨噬细胞的动力学特征。在嵌合体小鼠内纵向检测细胞侵袭,采用实时PCR定量分析视网膜炎性细胞因子水平。

试验性BRVO模型进行的三天内,组织学检查结果显示缺氧导致的组织结构改变与临时组织肿胀,伴有VEGF-A与缺氧诱导性因子1α(HIF-1α)表达和炎症因子水平的升高,随后视网膜内膜变薄。在缺氧早期,缺氧视网膜区域就能观察到明显的视网膜小胶质细胞的激活与循环巨噬细胞的募集活动,在第7天时达到峰值,并在28天内持续保持高活动水平, 促炎细胞因子水平增高。流式细胞仪检测显示CD68和MHCII在第3天开始表达,并且在第七天达到高峰。

试验性BRVO会引起缺氧和内层视网膜屏障的破坏,随后引起小胶质细胞激活和循环系统来源的巨噬细胞浸润。因此,针对小胶质细胞活化或巨噬细胞招募的靶点治疗或可减轻视网膜分支静脉阻塞引起的后遗症与退行性改变。

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    2017-10-03 tomyang96
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    2017-04-10 fusion
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    2017-04-01 zutt
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