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脂酶D3 (PLD3) 变体影响血管功能和炎症,影响内皮细胞和壁细胞. 这项研究揭示了PLD3在阿尔茨海默病的发病过程中的作用,特别是在血管重塑和粉样蛋白前体蛋白加工方面.

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科学领域:

  • 神经科学是一个神经科学.
  • 遗传学 遗传学 是一个
  • 血管生物学 血管生物学

背景情况:

  • 全基因组关联研究 (GWAS) 将单核酸多态 (SNP) 与晚发性阿尔茨海默病 (LOAD) 联系起来.
  • 一种罕见的脂酶D3 (PLD3) 变体 (p.A442A) 增加了LOAD风险的两倍,并与粉样前体蛋白 (APP) 处理有关.
  • 以前的研究表明PLD3在小鼠血管功能中的作用,但其在内皮细胞 (EC) 和壁细胞中的具体作用是未知的.

研究的目的:

  • 调查PLD3变种对血管功能和阿尔茨海默病 (AD) 发病的影响.
  • 使用小鼠模型和人类诱导多能干细胞 (iPSCs) 探索PLD3在内皮细胞 (ECs) 和壁细胞中的作用.

主要方法:

  • 利用了APP/PS1xPLD3淘汰赛 (KO) 的小鼠,并分析了皮质RNA测序 (RNA-seq) 数据.
  • 使用人类iPSC分化成EC和壁细胞,在2D和3D血管网络模型中培养.
  • 通过RNA-seq,免疫组织化学,细胞因子释放试验和电细胞基底阻抗传感 (ECIS) 评估了PLD3变异和淘汰效应,用于EC屏障功能.

主要成果:

  • 在APP/PS1xPLD3KO小鼠中,血管和炎症通路的下调,而蛋白质降解通路的上调.
  • 具有PLD3变异或淘汰的iPSC衍生EC显示细胞分裂和APP处理发生变化,影响AD-GWAS基因.
  • PLD3变异壁画细胞表现出破坏的细胞外矩阵重塑 (例如,FN1,MMP25).
  • 使用PLD3变体的3D血管模型显示了改变的INTERLEUKIN-8 (IL-8)释放,这表明血管重塑的含义.

结论:

  • 在小鼠中,PLD3显著影响血管功能和炎症,可能有助于阿尔茨海默氏症 (AD) 的发病.
  • 在人类iPSC衍生的血管模型中,PLD3调节EC增殖,APP处理和壁细胞矩阵组织.
  • 该PLD3变种可能会诱导血管重塑或不稳定,需要进一步调查潜在治疗向的潜在机制.