文章摘要
薛 璇,王 琪,石中华,赵 纯.miR-518d在正常妊娠及妊娠期糖尿病患者胎盘及血清中的表达研究[J].南京医科大学学报,2013,(11):1572~1575
miR-518d在正常妊娠及妊娠期糖尿病患者胎盘及血清中的表达研究
Investigation on the expression of miR-518d in the placenta and serum of gestational diabetes mellitus and normal pregnant women
投稿时间:2013-06-07  
DOI:10.7655/NYDXBNS20131121
中文关键词: miR-518d  妊娠期糖尿病  雌二醇  胎盘  过氧化物酶体增殖物激活受体α
英文关键词: miR-518d  GDM  estradiol  placenta  PPARα
基金项目:国家自然科学基金(81000258,81100436);江苏省自然科学基金(BK2010586)
作者单位
薛 璇 南京医科大学附属南京妇幼保健院产科,南京 江苏 210004 
王 琪 南京医科大学附属南京妇幼保健院产科,南京 江苏 210004 
石中华 南京医科大学附属南京妇幼保健院产科,南京 江苏 210004 
赵 纯 南京医科大学附属南京妇幼保健院产科,南京 江苏 210004 
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中文摘要:
      目的:检测正常妊娠及妊娠期糖尿病患者胎盘及血清中microRNA518d(miR-518d)的表达,探讨其在妊娠期糖尿病发病及诊断中的作用。方法:选择无妊娠并发症和合并症的足月剖宫产分娩产妇20例及妊娠期糖尿病足月剖宫产分娩产妇20例。分别收集两组的新鲜胎盘组织及母体血清,用Taqman实时荧光定量PCR方法检测两组miRNAs的变化。结果:miR-518d在妊娠期糖尿病胎盘中的表达(4.35 ± 0.88)显著高于对照组(1.04 ± 0.73)(P < 0.01),而其在妊娠期糖尿病血清中的表达水平(2.43 ± 1.07)也明显高于对照组(0.96 ± 0.88)(P < 0.05),生物信息学预测过氧化物酶体增殖物激活受体α(PPARα)3′UTR区含有miR-518d的结合位点,且胎盘miR-518d表达水平和血清雌二醇水平呈正相关(R2 = 0.759,r = 0.871)。结论:miR-518d可能通过调控PPARα基因参与妊娠期糖尿病的发病,有望成为妊娠期糖尿病的潜在诊断指标。
英文摘要:
      Objective:To investigate the expression level of miR-518d in the placenta and maternal serum of gestational diabetes mellitus and normal pregnant women. Methods:The expression of miR-518d in placenta and serum was measured by Taqman RT-PCR in 20 women with GDM and 20 women with normal term pregnancy. Results:Expression of miR-518d in placenta was significantly up-regulated in GDM group(4.35 ± 0.88)compared to control group(1.04 ± 0.73)(P < 0.01). Expression of miR-518d in serum was also up-regulated in GDM group(2.43 ± 1.07)compared to control group(0.96 ± 0.88)(P < 0.05). We also showed that PPARa was a direct target of miR-518d with a specific binding site at the seed sequence. And expression of miR-518d in the placenta was significantly positive correlated with the expression of serum E2(R2=0.759,r = 0.871). Conclusion:miR-518d is related with the mechanism of GDM and we suggest that upregulation of miR-518d may be associated with the pathogenesis of GDM via an effect on the regulation of PPARα expression.
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