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生物机械刺激促进了血管生长,尽管VEGFR-2抑制

Bronte Miller Johnson¹, Allison McKenzie Johnson¹, Michael Heim¹

¹Department of Biomedical Engineering, University of Alabama at Birmingham, 1824 6th Avenue South, Wallace Tumor Institute, Room 630A, Birmingham, AL, 35294, USA.

|December 10, 2023

概括

机械力量激活VEGFR-2,促进瘤中的血管生长,即使使用抑制剂. 这表明,新的抗血管性疗法应该考虑瘤微环境 (TME) 中的机械线索,以获得更好的疗效.

科学领域:

在瘤学瘤学.
生物医学工程生物医学工程
细胞生物学细胞生物学

背景情况:

血管新生对于瘤生长至关重要,需要新的血管来提供营养.
目前的抗血管性疗法针对VEGF和VEGFR-2,但在瘤微环境 (TME) 中经常失败.
这些疗法忽略了TME中的机械线索,这些线索也可能激活VEGFR-2.

研究的目的:

研究生物机械刺激对VEGFR-2激活和血管生成的作用.
在机械应变和VEGF刺激下分析VEGFR-2酸化模式.
在模拟TME的3D微组织模型中评估VEGFR-2抑制剂的疗效.

主要方法:

在Y1054/Y1059和Y1214残留物中分析VEGFR-2酸化.
用VEGF和/或拉伸性菌株刺激内皮细胞.
评估下游的 Src 表达式.
使用纤维素凝和微流体设备作为3DTME模型.

主要成果:

机械应变,单独或与VEGF,延长和增强VEGFR-2激活.
菌株和VEGF都激活了Src的表达.
机械应变促进了3D模型中的血管增长,即使有VEGFR-2抑制.

结论:

机械应变可以激活VEGFR-2,有助于TME中的血管生成.
了解生物机械和生物化学刺激是有效的抗血管生成疗法的关键.
单独使用VEGFR-2抑制剂不足以在机械应变的情况下阻止血管生成.

关键词:

血管新生的产生.内皮细胞是内皮细胞.机械生物学机械生物学压力应变是一种压力.瘤微环境是一个微环境.在VEGF中,VEGF是VEGF.在VEGFR-2的基础上,

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