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作 者:李杰[1] 周庆[2] 何孝军[2] 程永庆[2] 王东进[1]
机构地区:[1]南京医科大学鼓楼临床医学院胸心外科,南京210029 [2]南京大学医学院附属鼓楼医院胸心外科,南京210008
出 处:《中南大学学报(医学版)》2017年第10期1136-1142,共7页Journal of Central South University :Medical Science
摘 要:目的:研究miR-146b在急性Stanford A型主动脉夹层(Stanford type A aortic dissection,TAAD)患者外周血清及主动脉壁组织中的表达,探讨miR-146b在TAAD发病中的意义及机制。方法:将研究对象分为对照组(n=23)和TAAD组(n=27),收集所有研究对象的外周血清、术中主动脉壁组织和临床资料。运用实时荧光定量PCR(quantitative realtime PCR,qRT-PCR)检测各组外周血清及主动脉壁组织中miR-146b的表达水平。比较不同主动脉夹层风险级别的miR-146b水平,对miR-146b水平与TAAD患者主动脉夹层破裂风险进行相关性分析。运用DIANA LAB-TarBase 6.0数据库及TargetScan靶基因预测软件预测miR-146b相关靶基因。结果:TAAD组外周血清和主动脉壁组织中miR-146b表达水平均较对照组增高(P<0.001);中度风险和重度高危的TAAD患者外周血清和主动脉壁组织中miR-146b的表达水平较轻度风险患者明显增高(P<0.05);TAAD外周血清和主动脉壁组织中miR-146b差异表达与主动脉夹层高危风险呈正相关(r=0.862,0.872;P<0.05)。核因子κB1(nuclear factor kappa B1,NF-κB1)、肿瘤坏死因子受体相关因子6(tumor necrosis factor receptor-associated factor 6,TRAF6)、基质金属蛋白酶-16(matrix metalloproteinase 16,MMP16)和肌动蛋白2(actin alpha 2,ACTA2)为miR-146b的靶基因。Objective: To explore expression of miR-146b in peripheral blood serum and aortic wall tissues in patients with acute Stanford type A aortic dissection (TAM)), and to discuss the significance and underlying mechanisms. Methods: The subjects were divided into a control group (excluded relative aortic diseases) (n=23) and a TAAD group (n=27). The miR-146b levels of serum and aortic wail tissues were detected by quantitative real-time PCR (qRT-PCK). Serum miR-146b and aortic wall tissues miR-146b were compared among different risk TAAD groups. The correlations between miR-146b and severity of aortic dissection were analyzed. MiR- 146b related target genes were predicted by the DIANA LAB- TarBase 6.0 and TargetScan. Results" The expression levels of miR-146b in the serum and aortic wall tissues in the TAAD group were significantly elevated compared with those in the control group (P〈0.001). Compared with the mild risk group, the miR-146b levels of serum and aortic wall tissues were significantly higher in the moderate risk and severe risk groups (P〈0.05). The expression of miR-146b was positively correlated with the risk severity of TAM) patients (r=0.862, 0.872; P〈0.05). Nuclear factor kappa B1 (NF-~cBI), tumor necrosis factor receptor-associated factor 6 (TRAF6), matrix metalloproteinase 16 (MMP16) and actin alpha 2 (ACTA2) were miR-146b related target genes. Conclusion: The upregulation of miR-146b in peripheral blood serum and aortic wall tissues may contribute to the pathogenesis of TAAD and the severity of this disease.
关 键 词:miR-146b 主动脉夹层 核因子κB1 肿瘤坏死因子受体相关因子6 基质金属蛋白酶-16 肌动蛋白2
分 类 号:R543.1[医药卫生—心血管疾病]
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