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HTATIP2调节肢体缺血症患者单细胞中的动脉产生活性

Ashish S Patel¹, Francesca E Ludwinski¹, Angeles Mondragon¹

¹Academic Department of Vascular Surgery, South Bank Section, School of Cardiovascular and Metabolic Medicine & Sciences, King's BHF Centre of Research Excellence, King's College London, United Kingdom.

|October 17, 2023

概括

慢性肢体威胁性缺血症 (CLTI) 患者的单细胞/巨细胞由于HTATIP2增加而功能受损. 沉默HTATIP2拯救了它们的益动脉生成能力,为CLTI提供了潜在的细胞治疗策略.

科学领域:

再生医学是一种再生医学.
血管生物学血管生物学
细胞疗法细胞疗法

背景情况:

慢性肢体威胁性缺血症 (CLTI) 的细胞治疗显示出适度的疗效,可能是由于自身细胞受损.
亲动脉性单细胞/巨细胞 (Mo/MΦs) 在新血管化和动脉生成中起着至关重要的作用.

研究的目的:

为了调查来自CLTI患者的益动脉性Mo / MΦs的功能障碍.
阐明CLTI中Mo/MΦ功能障碍的潜在机制.
评估调节这些机制的治疗潜力.

主要方法:

从CLTI患者和健康对照中分离和表征益动脉性Mo/MΦs.
在体外和体内测试以评估新血管化和动脉生成能力.
对HTATIP2 (人类HIV-1 TAT交互蛋白-2) 的基因沉默和对血管/动脉调节剂和过程的下游影响的评估.

主要成果:

与对照组相比,CLTI Mo/MΦs的新血管化能力受损.
在CLTI Mo/MΦs中增加HTATIP2表达与抑制的血管生成/动脉生成有关.
沉默HTATIP2恢复了Mo/MΦ功能,增加了神经蛋白-1和血管蛋白-1的表达,并增强了内皮管的形成和光滑肌肉的增殖.
在体内,CLTI Mo/MΦs中的HTATIP2沉默通过增强的血管生成和动脉生成改善了四肢 perfusion.

结论:

来自CLTI患者的益动脉性Mo/MΦ功能受损,部分原因是HTATIP2升高.
对HTATIP2的ex vivo调节可以恢复对CLTI自身Mo/MΦs的治疗潜力.
针对HTATIP2是一个有前途的策略,可以提高CLTI患者的细胞治疗疗效.

关键词:

血管新生的产生.心血管疾病是什么心血管疾病巨细胞是一个巨细胞.单细胞 (Monocytes) 是一种单细胞.治疗方法治疗方法

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