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在外周动脉疾病中通过S100A8/S100A9调节巨细胞极化

Vijay Chaitanya Ganta^1,2, Min Choi¹, Charles R Farber³

¹Robert M. Berne Cardiovascular Research Center (V.C.G., M.C., B.H.A.), University of Virginia, Charlottesville.

|December 28, 2018

概括

巨细胞中的血管内皮生长因子-B (VEGF165b) 通过促进抗血管性M1类表型,损害了周围动脉疾病 (PAD) 的血流恢复. 这一发现揭示了改善PAD患者输液的新治疗点.

科学领域:

分子生物学
血管生物学
免疫学

背景情况:

周围动脉疾病 (PAD) 涉及肢体血流减少,导致缺血和组织损失,没有有效的医疗治疗来恢复输液.
血管内皮生长因子 (VEGF) - A疗法未能诱导血管生成并改善严重PAD的输液.
已知VEGF₁₆₅b抑制血管生成,但其在PAD巨细胞功能中的作用尚不清楚.

研究的目的:

调查VEGF₁₆₅b在外周动脉疾病 (PAD) 中调节巨细胞表型和功能的作用.
阐明VEGF₁₆₅b影响巨分化及其对缺血肌肉血管生成和 perfusion 恢复的影响机制.

主要方法:

使用关动脉绑定和切除,在体外低氧血清饥饿模型中建立了临床前PAD模型.
使用的技术包括激光多普勒输液成像,采用细胞转移,免疫斑块分析,ELISA,免疫染,流细胞测量,qPCR和RNA测序.
对VEGF₁₆₅b表达和VEGFR1信号的反应进行了检查.

主要成果:

与对照组相比,在PAD肌肉活检中观察到VEGF< sub>165b表达和M1类巨细胞的增加.
显示VEGF₁₆₅b可以抑制VEGFR1的激活,从而诱导一种类似M1的巨细胞表型,从而损害缺血肌肉中的新血管化.
通过RNA测序发现S100A8/S100A9是巨分极的下游VEGFR1调节者.

结论:

在巨细胞中增加的VEGF₁₆₅b表达驱动一种抗血管性M1类表型,直接阻碍血管生成并损害PAD的 perfusion恢复.
由VEGF₁₆₅b介导的VEGFR1抑制导致S100A8/S100A9诱导的流,促进M1类的表型,加剧缺血性肌肉再血管化.

关键词:

替代拼接血管新生诱导剂自律性沟通移动通信细胞间信号和蛋白质副沟通治疗药物

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