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从小到孕期新生儿的HUVEC中重塑染色质景观

Lingling Yan¹, Zhimin Zhou², Shengcai Chen²

¹Department of Pediatrics, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.

|April 22, 2025

概括

对于妊娠年龄来说小 (SGA) 与内皮功能障碍有关. 这项研究发现了SGA细胞的表观遗传变化,确定CD44是病理性血管生成的关键驱动因素,提供治疗点.

科学领域:

血管生物学血管生物学
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.
内皮细胞生物学内皮细胞生物学

背景情况:

对于妊娠年龄来说小 (SGA) 与心血管疾病和代谢综合征的风险增加有关.
内皮功能障碍是SGA已知的并发症,但其潜在机制尚未完全理解.

研究的目的:

研究导致SGA患者内皮功能障碍的分子和表观遗传机制.
为了确定关键的基因和途径,涉及病态血管生成在SGA相关的内皮功能障碍.

主要方法:

来自SGA个体的人类静脉内皮细胞 (HUVECs) 的表征.
全基因组转录和染色质可访问性概况 (ATAC-seq).
对增强剂调制和转录因子抑制的CRISPR干扰.

主要成果:

SGA-HUVECs表现出增强的血管生成,迁移,增殖和伤口愈合.
在SGA-HUVEC中观察到全球基因表达和染色质重塑.
由三种活性增强剂驱动的CD44的上调,可获得性增加,被确定为通过调节亲血管性基因和信号通路 (ERK1/2, eNOS) 的超血管生成的关键驱动因素.
激活蛋白-1 (AP-1) 被确定为调节CD44表达的关键转录因子.

结论:

表观遗传变化,特别是对调节CD44的增强剂增加的染色质可访问性,有助于SGA的病理血管生成.
向CD44表达或AP-1活性可能为SGA中的内皮功能障碍提供治疗策略.

关键词:

血管新生的产生.心脏病学心脏病学表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.

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