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失调的VE-cadherin/β-catenin表达介于扩张性心肌病的内皮细胞退化.

Romana Schäfer1, Dietmar Abraham, Patrick Paulus

  • 1Laboratory for Cardiovascular Research, Department of Anatomy, University of Vienna, Vienna, Austria.

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概括
此摘要是机器生成的。

在扩张性心肌病 (DCM) 中,内皮细胞生存受损,原因是减少了VE-cadherin/β-catenin,独立于VEGF. 向VE-cadherin可以治疗与DCM相关的EC病理.

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科学领域:

  • 心血管生物学 心血管生物学
  • 细胞生物学 细胞生物学
  • 分子医学是分子医学.

背景情况:

  • 血管内皮生长因子 (VEGF) -A,血管蛋白质 (Ang) 和VE-cadherin的相互作用调节了内皮细胞 (EC) 的存活率.
  • 心脏VEGF-A表达在扩张性心肌病 (DCM) 中降低,但VE-cadherin/Ang信号传递的作用尚不清楚.

研究的目的:

  • 为了研究VE-cadherin/beta-catenin和angiopoietin信号在DCM患者的心肌中的功能.
  • 确定VE-cadherin/β-catenin,血管蛋白和DCM中的内皮细胞退化之间的关系.

主要方法:

  • 在DCM,缺血性心肌病 (ICM) 和使用实时RT-PCR,西方斑点和免疫细胞化学的对照对象中检查了VE-cadherin/beta-catenin,Ang-1,Ang-2和Tie-2的心肌表达.
  • 通过传输电子显微镜 (TEM) 量化内皮细胞退化.
  • 在培养细胞中利用RNA干扰和VEGF操纵来探索分子相互作用.

主要成果:

  • 在DCM中,VE-cadherin/β-catenin的表达显著下调,但在ICM中却没有.
  • 在DCM和ICM中,Ang-2表达是下调的,而Tie-2蛋白是上调的.
  • 与ICM相比,DCM中观察到更高的内皮细胞退化率,VE-cadherin基因沉默模仿DCM相关的EC病理.

结论:

  • 在DCM中,内皮细胞生存受损,与VE-cadherin/beta-catenin功能障碍有关,可能与VEGF无关.
  • 向VE-cadherin为DCM相关的内皮细胞病理学提供了潜在的治疗策略.