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由于Phd2的哈普洛缺陷而导致的巨细胞倾斜,通过诱导动脉生成来预防缺血

Yukiji Takeda¹, Sandra Costa, Estelle Delamarre

¹Laboratory of Molecular Oncology and Angiogenesis, Vesalius Research Center, VIB, Leuven B-3000, Belgium.

|October 11, 2011

概括

酸酶域2 (PHD2) 缺陷通过促进M2类巨细胞极化来增强附带动脉生长. 这改善了血液的流动,并防止了缺血条件下的组织损伤,这表明了新的治疗策略.

科学领域:

血管生物学血管生物学
缺血病研究缺血病研究
巨细胞生物学

背景情况:

甲基氧酶域2 (PHD2) 作为氧气传感器,在缺氧期间调节血管形成.
PHD2在动脉生成中的作用,即附带动脉的生长,仍然在很大程度上未被探索.

研究的目的:

通过后肢缺血模型,研究PHD2在附带动脉生长中的功能.
阐明PHD2影响动脉生成和组织 perfusion 的机制.

主要方法:

在后肢缺血模型中利用Phd2(+/-) 鼠标来研究附带动脉发育.
分析了巨细胞两极分化,动脉动脉因子释放和光滑肌肉细胞的招募.
研究了NF-κB通路在PHD2-介导动脉生成中的作用.

主要成果:

Phd2(+/-) 小鼠表现出预先形成的附带动脉,保持四肢 perfusion 和防止死后缺血.
动脉生成因M2型巨细胞的扩张和动脉生成因子的释放增加而增强.
在巨细胞中删除一个Phd2等位基因诱导了亲动脉原性表型,涉及NF-κB通路激活.

结论:

通过控制巨细胞分化,PHD2对动脉发生和动脉稳定有关重要的调节.
在巨细胞中准PHD2为缺血性疾病提供了潜在的治疗方法.

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