神经前体衍生的阿佩林控制尖端细胞的行为和血管模式
Julian Malchow1, Jean Eberlein1, Wei Li1
1Faculty of Biology, Cell Signaling and Dynamics, Philipps-University of Marburg, Marburg, Germany.
Science advances
|July 5, 2024
概括
神经原生细胞分泌阿佩林,这是一种分子,在血管形成 (血管生成) 过程中对血管尖端细胞指导至关重要. 这种神经血管交叉交谈对于适当的尖端细胞功能和网络发展至关重要.
科学领域:
- 神经科学是一个神经科学.
- 发展生物学 发展生物学
- 血管生物学 血管生物学
背景情况:
- 血管生成涉及血管尖端细胞指导新的血管形成.
- 在血管尖端细胞中发现了Aplnr的连接体Apelin,这表明它在调节发芽血管生成方面发挥了作用.
- 阿佩林在血管生成中的来源和精确功能仍然不完全理解.
研究的目的:
- 为了研究阿佩林在调节血管尖端细胞在生长血管生成过程中的作用.
- 确定影响血管生成的Apelin细胞源.
- 为了阐明尖端细胞中Apelin调节的信号通路.
主要方法:
- 在背部神经管中识别阿佩林表达细胞.
- 在阿佩林缺陷模型中分析血管尖端细胞迁移和延长.
- 基因操纵以恢复神经或血管区的阿佩林表达.
- 功能性测试用于评估尖端细胞行为 (例如,filopodia形成).
- 基因相互作用研究和信号通路报告者的分析 (PI3K,ERK).
主要成果:
- 确定了一种表达阿佩林的神经前体细胞群.
- 血管尖端细胞向这些神经前代细胞和沿着这些神经前代细胞迁移.
- 恢复神经阿佩林表达,但不是血管,在突变者中挽救了血管性缺陷.
- 尖端细胞的延长和filopodia形成需要阿佩林信号.
- 阿佩林信号调节了尖端细胞中的酸酸3-激酶和细胞外信号调节激酶通路.
结论:
- 来自神经原生细胞的阿林信号传递,在发芽血管生成过程中对血管尖端细胞功能至关重要.
- 这项研究揭示了一种由Apelin调解的新型神经血管交叉交谈机制.
- 阿佩林在调节PI3K/ERK信号传递中的作用对于活体中尖端细胞的行为至关重要.
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