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相关概念视频

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Blood vessel formation starts early during embryonic development, around day 7. In the extraembryonic yolk sac, mesodermal precursor cells called hemangioblast proliferate and differentiate into angioblast. Angioblasts express vascular endothelial growth factor receptor 2 or VEGFR2, which binds VEGF-A, a proangiogenic factor, guiding blood vessel formation. VEGF signaling promotes angioblasts to form a blood island in the developing embryo. Angioblasts further differentiate, giving rise to...
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Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
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相关实验视频

Updated: May 6, 2026

Murine Aortic Crush Injury: An Efficient In Vivo Model of Smooth Muscle Cell Proliferation and Endothelial Function
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可溶性瘤缩因子-α受体1的肌肉内基因转移激活了血管内皮生长因子受体,并加速了后肢缺血病的老鼠模型中的血管生成.

Masahiro Sugano1, Keiko Tsuchida, Naoki Makino

  • 1Department of Molecular and Cellular Biology, Division of Molecular and Clinical Gerontology, Medical Institute of Bioregulation, Kyushu University, 4546 Tsurumihara, Beppu, Oita, 874-0838, Japan. massy@tsurumi.beppu.kyushu-u.ac.jp

Circulation
|February 19, 2004
PubMed
概括
此摘要是机器生成的。

使用可溶性TNF-α受体1 (sTNFR1) 等离子体抑制瘤坏死因子-α (TNF-alpha),增强了血管内皮生长因子受体 (KDR/flk-1) 激活,并在大鼠后肢缺血模型中促进了血管生成.

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科学领域:

  • 血管生物学 血管生物学
  • 基因治疗 基因治疗
  • 缺血症研究 缺血症研究

背景情况:

  • 瘤坏死因子-α (TNF-α) 通过非激活血管内皮生长因子 (VEGF) 受体来抑制内皮细胞的增殖.
  • 可溶性TNF-α受体1 (sTNFR1) 作为TNF-α对抗剂.
  • 这项研究研究了sTNFR1对VEGF受体 (KDR/flk-1) 和后肢缺血中的血管生成的影响.

研究的目的:

  • 评估sTNFR1表达等离子体对KDR/flk-1的影响和后肢缺血的老鼠模型中的血管生成.
  • 为了确定抑制TNF-α活性是否可以改善缺血组织中的血管性反应.

主要方法:

  • 后肢缺血是通过切除大腿动脉来诱导大鼠的.
  • sTNFR1或LacZ等离子体被注射到补充肌肉中.
  • 测量包括TNF-alpha生物活性,KDR/flk-1mRNA和酸化,VEGF水平和毛细血管密度.

主要成果:

  • sTNFR1等离子体抑制了缺血肌肉中TNF-α生物活性的增加.
  • 在接受sTNFR1治疗的肌肉中,KDR/flk-1mRNA和氨酸酸化显著增加.
  • 在21天后,在sTNFR1等离子体转移的肌肉中,毛细血管密度显著更高.

结论:

  • TNF-alpha可能抑制KDR/flk-1激活,并在后肢缺血中损害血管生成.
  • sTNFR1基因转移调节KDR/flk-1并通过抑制TNF-alpha来加速血管生成.
  • 当地的sTNFR1基因转染为外周缺血性疾病提供了潜在的治疗策略.