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作 者:刘高[1] 杨丽霞[1] 朱国富[1] 刘宏[1] 邹继红[1] 郭瑞威[1] 齐峰[1] 石燕昆[1]
机构地区:[1]成都军区昆明总医院心内科,云南昆明650032
出 处:《中华高血压杂志》2013年第7期671-674,共4页Chinese Journal of Hypertension
摘 要:目的探讨微小RNA-155(miR-155)对血管紧张素Ⅱ(AngⅡ)诱导的原代培养的小鼠主动脉平滑肌细胞增殖的影响。方法用贴壁法原代培养C57小鼠主动脉血管平滑肌细胞,进行miR-155转染,分别用AngⅡ10-6mol/L(空白对照)、miR-155+AngⅡ(10-6mol/L)(miR-155过表达)和miR-155阴性+AngⅡ(10-6mol/L)(miR-155阴性对照)干预细胞,采用实时荧光定量PCR检测miR-155转染24h后的转染效率。用免疫荧光法检测干预48h后细胞增殖情况,以增殖细胞核与总数量细胞核相比较计算增殖的效率,比较3组miR-155表达水平和细胞增殖情况。结果对血管平滑肌细胞进行转染后,与空白对照组及miR-155阴性对照组比较,miR-155过表达组miR-155表达水平明显升高(P<0.01),血管平滑肌细胞增殖明显减少[(26.40±5.03)%比(66.80±5.63)%,(58.40±5.18)%,P<0.05]。结论 miR-155可抑制AngⅡ诱导的原代培养的小鼠主动脉血管平滑肌细胞的增殖。Objective To explore the effects of microRNA(miR)-155 on mice derived primary aortic vascular smooth muscle cells proliferation induced by angiotensin Ⅱ (Ang Ⅱ ). Methods The aortic vascular smooth muscle cells derived from C57 mice were cultured by adherent method. Cells were treated as following: Ang H 10^-6 mol/L (blank control); miR 155+Ang Ⅱ (10^-6 mol/L)(miR-155) and miR-155 negative+Ang Ⅱ (10^-6 mol/L) (miR-155 negative control). Twenty-four hours after transfection, the miR-155 transfection efficiency was examined by real- time PCR. The cell proliferation was detected by immunofluorescence 48 hours later. The ratio of proliferating nuclei and the total number of nuclei was used to verify the proliferation efficiency. The miR-155 levels and the cell proliferation status of the three groups were compared. Results After transfection, compared to blank control group and miR-155 negative group, the miR-155 level was significantly increased in miR-155 group ( P〈0.01), the vascular smooth muscle cells proliferation was significantly reduced [( 26.40±5.03 )% vs ( 66.80±5.63 ) %, (58.40±5.18)%, P〈0.05]. Conclusion miR-155 can inhibit aortic vascular smooth muscle cells proliferation induced by Ang Ⅱ in mouse derived primary aortic vascular smooth muscle cells.
关 键 词:微小RNA-155 血管紧张素Ⅱ 血管平滑肌细胞 增殖
分 类 号:R543[医药卫生—心血管疾病]
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