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热休克蛋白70与胎盘血管病中内皮激活的相关研究 被引量:1

Study of Relationship between Hsp70 and Endothelial Activation inPlacental Vascular Diseases
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摘要 目的:进一步阐明胎盘血管病(PVD)的发病机制。方法:选取胎盘血管病组(研究组)与正常孕妇(对照组)两组标本,选择应用寡核苷酸芯片技术筛选出差异表达水平较高的基因,定量PCR和Western-blot验证表达,并应用免疫组化检测定位。结果:与对照组相比,HspA1A和HspA6表达水平显著改变,且共同编码热休克蛋白(Hsp70);Hsp70在胎盘微血管中主要表达在内皮细胞和平滑肌细胞;研究组与对照组相比,Hsp70mRNA和蛋白的表达均增高(P<0.05);Hsp70mRNA和蛋白的表达均与胎儿出生时的体重呈负相关(P<0.05)。结论:Hsp70在PVD的发病机制中是极其重要的,Hsp70高表达可能引起了内在的免疫应答和炎性反应。 目的:进一步阐明胎盘血管病(PVD)的发病机制。方法:选取胎盘血管病组(研究组)与正常孕妇(对照组)两组标本,选择应用寡核苷酸芯片技术筛选出差异表达水平较高的基因,定量PCR和Western-blot验证表达,并应用免疫组化检测定位。结果:与对照组相比,HspA1A和HspA6表达水平显著改变,且共同编码热休克蛋白(Hsp70);Hsp70在胎盘微血管中主要表达在内皮细胞和平滑肌细胞;研究组与对照组相比,Hsp70mRNA和蛋白的表达均增高(P&lt;0.05);Hsp70mRNA和蛋白的表达均与胎儿出生时的体重呈负相关(P&lt;0.05)。结论:Hsp70在PVD的发病机制中是极其重要的,Hsp70高表达可能引起了内在的免疫应答和炎性反应。
出处 《实用妇产科杂志》 CAS CSCD 北大核心 2010年第3期222-224,241,共4页 Journal of Practical Obstetrics and Gynecology
基金 国家自然科学基金项目(编号:30471825)
关键词 基因芯片 热休克蛋白70 内皮激活 胎盘血管病 Gene arrays Heat shock protein70 Endothelial activation Placental vascular disease
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参考文献10

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同被引文献8

  • 1Zhao R, Houry WA. Molecular interaction network of the HspgO chaper- one system. Adv Exp Med Biol,2007,594:27-36.
  • 2Strethapakdi M,Liu F,Tavorath R,et al. Inhibition of Hsp90 function by ansamycins causes retinoblastoma gene product-dependent GI arrest. Cancer Res ,2000,60:3940-3946.
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  • 4Deb TB,Zuo AH, Wang Y,et al. Pnck induces ligand-independent EGFR degradation by probable perturbation of the Hsp90 chaperone complex. Am J Physiol Cell Physiol,2011,300 : C1139-1154.
  • 5Rangaraju S, Madorsky I, Pileggi JG, et al. Pharmacological induction of the heat shock response improves myelination in a neuropathie model. Neurobiol Dis,2008,32 : 105-115.
  • 6Luo S, Zhang B, Dong XP, et al. HSP90 beta regulates rapsyn turnover and subsequent AChR cluster formation and maintenance. Neuron,2008, 60:97-110.
  • 7赵勇,耿素敏,张瑞青,王景阳,吴晶.妊高征患者血清HSP70水平的表达及意义[J].中国卫生检验杂志,2009,19(1):135-136. 被引量:11
  • 8耿素敏,赵勇,严真真.血清热休克蛋白70在重度子痫前期合并HELLP综合征中的价值探讨[J].中国医药导刊,2009,11(12):2100-2101. 被引量:4

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