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通过Prokineticin 2- Prokineticin受体1通路调节血管生成

Shu Meng¹, Qilin Gu¹, Xiaojie Yang¹

¹Center for Cardiovascular Regeneration, Department of Cardiovascular Sciences, Houston Methodist Research Institute, TX.

|March 17, 2018

概括

TBX20是一种通过PROK2-PROKR1通路调节血管生成的新型转录因子. 这一发现为涉及异常血管形成的疾病提供了新的治疗点.

科学领域:

心血管生物学
分子生物学
发育生物学

背景情况:

血管新生对于胚胎发育和疾病病理学至关重要.
转录因子TBX20对于胚胎发育至关重要,并与先天性心脏病有关.
TBX20在血管生成中的特定作用仍未被描述.

研究的目的:

研究TBX20在血管生成中的作用.
确定参与血管生成的TBX20下游点.
探索TBX20血管生成途径的治疗潜力.

主要方法:

在血管生成 (体外和体内) 中使用功能损失和功能增益方法来研究TBX20.
使用血管生成基因阵列来识别TBX20的下游目标.
在小鼠模型和斑马鱼中验证的结果,包括基因淘汰和救援实验.

主要成果:

显著降低 prokineticin 2 (PROK2) 表达,并影响内皮细胞迁移和体外血管生成.
在小鼠模型中,TBX20缺乏减少了PROK2表达和内插血管生成.
在斑马鱼中增强了PROK2的血管生成和血液流的恢复;tbx20和prok2 / prok1a的干扰损害了血管生成,在prok2 / prok1a过度表达时观察到救援.

结论:

通过PROK2-PROKR1途径确定TBX20为血管生成的新型调节剂.
发现了一种支持血管内皮生长因子的TBX20-PROK2-PROKR1信号级联.
提出这种途径作为血管生成相关疾病的潜在治疗点.

关键词:

与G蛋白结合的新血管化,生理周围动脉疾病接收器

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