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HDAC2调控MiR199a-3p对大鼠心衰模型中心肌细胞凋亡的影响
石树文,田雯,陈聪,向龙
0
(成都市第一人民医院儿科)
摘要:
【摘要】 目的 探讨HDAC2调控MiR199a3p对大鼠心衰模型中心肌细胞凋亡的影响。 方法 选取清洁级健康成年雄性(spraguedawley,SD)大鼠40只,随机分为心衰组(HF组,20只)、假手术组(Sham组,10只)和空白对照组(无任何处理,Blank组,10只)3组。H&E 染色用于心脏大体形态分析;QPCR方法检测HDAC2、HDAC3、HDAC4、miR199a3p及其下游基因p53表达水平;western blot方法检测HDAC2及P53蛋白表达水平;染色质免疫共沉淀结合PCR(ChIPPCR)技术检测HDAC2与miR199a-3p启动子结合水平。 结果 与Sham组及Blank组对比,HF组大鼠心肌细胞明显肥厚。HDAC2 mRNA、p53 mRNA水平HF组显著高于Sham组及Blank组(P<0.05)。miR199 a3p mRNA水平HF组较Sham组及Blank组明显下降(P<0.05)。p53 mRNA、HDAC2 mRNA、miR199 a-3p mRNA表达水平Sham组与Blank组比较差异无统计学意义(P>0.05)。HDAC3及HDAC4mRNA表达水平在各组间差异均无统计学意义(P>0.05),HDAC2蛋白、p53蛋白HF组显著高于Sham组及Blank组(P<0.05),Sham组及Blank组比较差异无统计学意义(P>0.05)。HF组中HDAC2与miR199a-3p启动子结合水平较Sham组及Blank组明显升高(P<0.05),而HDAC3及HDAC4 mRNA水平在各组中无显著差异(P>0.05)。 结论 大鼠心衰模型中,组蛋白去乙酰化酶HDAC2介导miR199a-3p低表达,进而引起凋亡标志物p53表达上调。
关键词:  心力衰竭  组蛋白去乙酰化酶  miR199a-3p  p53
DOI:
基金项目:国家卫计委医药卫生科技发展研究中心;成都市科学技术局
HDAC2 regulates mir199a-3P on the apoptosis of central myocytes in rat heart failure model
SHI Shuwen,TIAN Wen,CHEN Cong,XIANG Long
(Department of Pediatrics, The First Hospital of Chengdu)
Abstract:
【Abstract】 Objective To investigate the effect of HDAC2 on the apoptosis of cardiac myocytes in rat heart failure model. Methods 40 healthy adult male (Sprague Dawley, SD) rats were randomly divided into HF group (20 rats), sham operation group (10 rats) and blank control group (10 rats, blank group). H & E staining was used for the analysis of cardiac gross morphology. QPCR was used to detect the expression level of HDAC2, HDAC3, HDAC4, mir199a 3P and their downstream gene p53. Western blot was used to detect the expression level of HDAC2 and p53 protein. The chromatin immunoprecipitation combined with PCR (chip PCR) was used to detect the binding level of HDAC2 and mir199a 3P promoter. Results Compared with sham group and blank group, myocardial cells in HF group were significantly hypertrophied. The levels of HDAC2 mRNA and p53 mRNA in HF group were significantly higher than those in sham group and blank group (P<0.05). The level of mir199a 3P mRNA in HF group was significantly lower than that in sham group and blank group (P<0.05). There was no significant difference in the expression levels of p53 mRNA, HDAC2 mRNA and mir199a 3P mRNA between sham group and blank group (P>0.05). There was no significant difference in the expression level of HDAC3 and hdac4mrna between the groups (P>0.05). The expression levels of HDAC2 protein and p53 protein in HF group were significantly higher than those in sham group and blank group (P<0.05). There was no significant difference between sham group and blank group (P>0.05). The binding level of HDAC2 and mir199a 3P promoter in HF group was significantly higher than that in sham group and blank group (P<0.05), but there was no significant difference in the levels of HDAC3 and HDAC4 mRNA in each group (P>0.05). Conclusion In the rat model of heartfailure, a histone deacetylase,medicates the tow expression of miR199a, which leads to the up regulation of p53, an apoptosis maker.
Key words:  Heart failure  Histone deacetylase  mir199a-3p  p53

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