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相关概念视频

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Mechanism of Angiogenesis

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Assessment and Characterization of Hyaloid Vessels in Mice
08:22

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原XVIII的损失增强了动脉样硬化中的新血管化和血管透性.

Karen S Moulton1, Bjorn R Olsen, Silvia Sonn

  • 1Vascular Biology Research Program, Department of Surgery, Children's Hospital Medical Center, 300 Longwood Ave, Boston, MA 02115, USA. karen.moulton@childrens.harvard.edu

Circulation
|August 18, 2004
PubMed
概括

原XVIII的损失通过增加血管生长和泄漏,促进动脉样硬化. 这种底层膜蛋白质甘氨酸通常会抑制vasa vasorum延伸,保持血管完整性.

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相关实验视频

Last Updated: Jul 19, 2026

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08:22

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Published on: May 15, 2019

Using En Face Immunofluorescence Staining to Observe Vascular Endothelial Cells Directly
06:09

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科学领域:

  • 血管生物学 血管生物学
  • 动脉样硬化研究 动脉样硬化研究
  • 细胞外矩阵生物学 细胞外矩阵生物学

背景情况:

  • 斑块新血管化有助于动脉样硬化,但其调节不清楚.
  • 原XVIII及其片段内静氨酸在血管底层膜中大量存在.
  • 原XVIII被假定可以抑制vasa vasorum的增殖和内密延伸.

研究的目的:

  • 研究原XVIII在调节动脉样硬化和血管透性的作用.
  • 为了确定原XVIII缺乏是否会在小鼠模型中加剧动脉样硬化.

主要方法:

  • 生成的原XVIII-Knockout (Col18a1(-/-)) 小鼠与阿波利波蛋白E缺陷 (ApoE(-/-)) 小鼠交叉.
  • 在胆固醇饮食后评估了大动脉动脉瘤覆盖范围,脂质积累和vasa vasorum新血管化.
  • 量化了内皮细胞生长和测量了血管透率.

主要成果:

  • ApoE ((-/-);Col18a1 ((-/-) 和ApoE ((-/-);Col18a1 ((+/-) 的小鼠与对照组相比,表现出动脉瘤和脂质积累的增加.
  • 在淘汰性大动脉中观察到更广泛的血管和亲密新血管化.
  • 血管透性增强,即使有异性失去了原XVIII.

结论:

  • 原XVIII保持了血管透性,这是以前未知的功能.
  • 原XVIII的损失通过基因剂量依赖的机制增强动脉形成和动脉样硬化期间的血管透性.