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作 者:徐建国[1] 杨超[1] 邢新[1] 戴海英[1] 方硕[1] 孙肇晟[1]
机构地区:[1]第二军医大学附属长海医院整形外科,上海200433
出 处:《中国美容整形外科杂志》2016年第4期238-241,共4页Chinese Journal of Aesthetic and Plastic Surgery
基 金:国家自然科学基金(81272119)
摘 要:目的研究上调婴幼儿血管瘤内皮细胞miR-206水平对细胞增殖、凋亡和侵袭能力的影响。方法通过CD31磁珠提取婴幼儿血管瘤内皮细胞,经转染miR-206模拟物提高HemECs细胞内miR-206水平,研究miR-206对该细胞功能的影响。以cck-8法检测细胞增殖能力的改变,AV-PI凋亡试剂盒经流式细胞仪检测凋亡水平变化,并经Transwell侵袭实验检测侵袭能力变化。结果转染miR-206模拟物进入HemECs细胞内48 h后,能够明显抑制细胞增殖,抑制率为(34.2±6.8)%;转染48 h后相比于对照组(1.7±1.6)%的凋亡细胞比率,miR-206模拟物组细胞凋亡比率提高到(23.9±5.1)%,差异具有统计学意义;转染后24 h侵袭实验显示,细胞穿透Transwell小室至下室面细胞数在对照组为30.3±2.4,在miR-206模拟物组细胞数减少至14.3±3.0。结论上调HemECs细胞内miR-206水平可明显抑制细胞增殖,增加细胞凋亡水平,减少细胞侵袭能力。提示miR-206可能通过调节瘤体细胞生物活性,对婴幼儿血管瘤疾病进程起到重要的调控作用。Objective To investigate the effect of miR-206 up-regulation on cell proliferation, apoptosis and invasion ability of infantile hemangioma endothelial cells (HemECs). Methods HemECs was isolated from infantile hemangioma digestion tissue by CD31 magnetic bead, then the miR-206 was up-regulated by miR-206 mimics transfection. The apoptosis of HemECs was examined using Annexin V-FITC/PI by flow cytometry and cell proliferation was detected by cck-8 assay method. Invasion ability was determined by Transwell invasion assay. Results The proliferation of HemECs was significantly inhibited after miR-206 mimics transfected into HemECs at 48h, the inhibit rate was (34.2±6. 8)%. Concerning transfection within the group of miR-206 mimics compared with the control group, the apoptosis level elevated from (1.7 ±1.6)% to (23.9± 5.1 )% after miR-206 mimics transfected into HemECs at 48 h. Matrigel invasion assay demonstrates that, within the group of miR-206 mimics transfection compared with the control group, the number of cells at the opposite surface of Transwell bottom decreased from 30.3 ±2.4 to 14.3 ± 3.0. Conclusion The miR-206 level in up-regulated HemECs could obviously inhibit cell proliferation ability, elevate the apoptosis level and decrease invasive ability. MiR-206 may have important regulation effect on pathogenesis of infantile hemangioma through adjusting HemECs' biological activation.
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