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维纳综合征衍生的巨细胞中的逆转移子在动脉样硬化模型中触发I型干扰素依赖性炎症

Sudip Kumar Paul¹, Motohiko Oshima², Ashwini Patil³

¹Department of Regenerative Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.

Nature communications

|June 10, 2024

概括

沃纳综合征 (WS) 患者由于巨细胞功能障碍而发展动脉样硬化. 抑制WS巨细胞中的I型干扰素信号传递可能会治疗这种情况.

科学领域:

心血管生物学心血管生物学
细胞机制细胞机制
遗传学与衰老的关系

背景情况:

动脉样硬化是维纳综合征 (WS) 死亡的主要原因.
在WS中驱动动动脉硬化的细胞机制尚未完全理解.
WS是一种与遗传不稳定性相关的过早衰老疾病.

研究的目的:

为了研究维纳综合征中的动脉样硬化机制.
为研究WS相关心血管疾病建立一个体外模型.
为了确定WS动脉样硬化的潜在治疗点.

主要方法:

开发了一种体外共同培养系统,使用诱导多能干细胞衍生的巨细胞 (iMφs),血管内皮细胞 (iVECs) 和血管光滑肌细胞 (iVSMCs).
利用转录学和开放色素分析来研究WS细胞中的细胞变化.
研究了I型干扰素信号传递和可逆转移元件的作用.

主要成果:

在共同培养中,WS巨诱导了内皮功能障碍和光滑肌肉细胞合成表型.
华氏体巨细胞显示I型干扰素信号加速和染色体可访问性降低.
可逆转移的元素激活了WS巨细胞中的DHX58依赖RNA传感.
沉默WS巨细胞中的I型干扰素信号,挽救了细胞功能,并减少了衰老.

结论:

宏细胞特异性I型干扰素信号传递是维纳综合征中动脉样硬化的关键驱动因素.
针对巨细胞中的I型干扰素信号提供了WS患者潜在的治疗策略.
这项研究提供了关于细胞衰老和心血管疾病机制的见解.

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