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国家自然科学基金(30801271)

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Staurosporine诱导RGC-5细胞分化作用的研究
2008年
目的观察Staurosporine是否可以诱导视网膜神经节细胞-5(RGC-5)的分化。方法正常培养RGC-5细胞,应用500nmol/L Staurosporine诱导RGC-5细胞分化,并在诱导后不同时间段连续观察细胞形态的变化。应用免疫荧光检测视网膜神经节细胞(RGCs)阳性标志因子Thy-1和Brn-3的表达,应用Western Blot、RT-PCR分别定量检测诱导分化后RGC-5细胞中的Thy-1和Brn-3蛋白表达及mRNA的转录情况。结果应用500nmol/L Staurosporine诱导后的RGC-5形态上表现出增生停止,胞体周围纤长轴突生长,轴突末端可见类似突触结构。500nmol/L Staurosporine可以诱导RGC-5细胞中RGCs阳性标志因子Thy-1和Brn-3转录及表达上调。结论500nmol/L Staurosporine可以有效地诱导RGC-5细胞向成熟RGCs分化。
李光宇范斌李亚萍崔极哲
关键词:STAUROSPORINE细胞分化THY-1
Calcium Overload Is A Critical Step in Programmed Necrosis of ARPE-19 Cells Induced by High-Concentration H_2O_2被引量:9
2010年
Objective Oxidative stress plays an important role in retinal pigmental epithelium (RPE) death during aging and the development of age-related macular degeneration.Although early reports indicate that reactive oxygen species (ROS) including H2O2 can trigger apoptosis at lower concentrations and necrosis at higher concentrations,the exact molecular mechanism of RPE death is still unclear.The purpose of this study was to investigate the molecular pathways involved in RPE death induced by exogenous ROS,especially at higher concentrations.Methods Cultured ARPE-19 cells were treated with H2O2 at different concentrations and cell viability was measured with the MTT assay.Cell death was morphologically studied by microscopy using APOPercentage assay and PI staining.Furthermore,the impact of oxidative stress on ARPE-19 cells was assessed by HO-1 and PARP-1 Western blotting and by the protection of antioxidant EGCG.Calcium influx was determined using the fura-2 calcium indicator and the role of intracellular calcium overload in ARPE-19 cell death was evaluated following cobalt treatment to block calcium effects.Results H2O2 reduced the viability of ARPE-19 cells in a concentration-dependent manner,which was presented as a typical s-shaped curve.Cell death caused by high concentrations of H2O2 was confirmed to be programmed necrosis.Morphologically,dying ARPE-19 cells were extremely swollen and lost the integrity of their plasma membrane,positively detected with APOPercentage assay and PI staining.24-hour treatment with 500 ?mol/L H2O2 induced remarkable up-regulation of HO-1 and PARP-1 in ARPE-19 cells.Moreover,antioxidant treatment using EGCG effectively protected cells from H2O2-induced injury,increasing cell viability from 14.17%±2.31% to 85.77%±4.58%.After H2O2 treatment,intracellular calcium levels were highly elevated with a maximum concentration of 1200nM.Significantly,the calcium channel inhibitor cobalt was able to blunt this calcium influx and blocked the necrotic pathway,rescuing the ARPE-19 cell fr
GUANG-YU LI BIN FAN YONG-CHEN ZHENG
关键词:NECROSIS
PARP-1在光诱导视网膜神经节细胞凋亡中的作用
2008年
目的研究核酶PARP-1在光诱导的视网膜神经节细胞(RGCs)凋亡中的作用。方法应用1000 Lux光诱导视网膜神经节细胞-5(RGC-5)光损伤模型;利用MTT、APOPercentageTM实验及原位TUNEL确定光诱导RGC-5细胞死亡的模式;通过半定量RT-PCR和Western blot方法评估光对RGC-5细胞中核酶PARP-1表达的影响;探讨PARP-1抑制剂尼克酰胺和NU1025对光损伤中RGC-5细胞的保护作用。结果1000 Lux光以时间依赖的方式降低体外培养的RGC-5细胞活性,光暴露4d明显诱导RGC-5细胞凋亡。RGC-5细胞光损伤导致核酶PARP-1转录和表达的上调(F=224.59,P<0.01,n=12,ANOVA,Dunnett t test),PARP-1抑制剂尼克酰胺和NU1025显著提高细胞活性(F=312.87,P<0.01,n=12,ANOVA,Dunnett t test)。结论1000 Lux光可以诱导体外培养的RGC-5细胞凋亡,核酶PARP-1在该细胞凋亡分子机制中起重要作用。
李光宇范斌
关键词:光损伤细胞凋亡视网膜神经节细胞PARP-1
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