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孕前胎儿编程通过DNA甲基化使后代易患肝硬化症

Huixi Chen¹, Sisi Luo², Xiuyu Deng³

¹The International Peace Maternal and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200000, China; Shanghai Key Laboratory of Reproduction and Development, Shanghai 200011, China; Research Units of Embryo Original Diseases, Chinese Academy of Medical Sciences, Shanghai 200030, China; Key Laboratory of Reproductive Genetics (Ministry of Education), Women's Hospital, Zhejiang University School of Medicine, Hangzhou 310000, China; State Key Laboratory of Cardiology, Shanghai 200000, China; Shanghai Key Laboratory of Embryo Original Diseases, Shanghai, 200030, China.

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|April 22, 2024

概括

孕产妇产前导致后代代谢障碍,包括肥胖,这是由于影响脂质代谢的表观遗传变化造成的. 早期干预可以减轻这些终身健康风险.

科学领域:

发育生物学是发展生物学.
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.
代谢障碍代谢障碍代谢障碍

背景情况:

"成年人疾病的双胞胎和胚胎-胎儿起源"假说将早期生活条件与成年人的慢性疾病联系起来.
孕产妇前 (PE) 是一种妊娠并发症,可能会为代谢功能障碍的后代进行编程.

研究的目的:

为了研究发育变化和代谢障碍的潜在表观遗传机制,从先兆子 (PE) 计划怀孕后代.
描述母亲PE后后代的长期代谢后果.

主要方法:

使用一种类似于子宫的小鼠模型,由Nω-Nitro-l-arginine甲基乙烯化物 (L-NAME) 诱导.
在年轻和年长的后代上进行了脂质分析,组织学,间接热量测量,mRNA测序和火烧测序.
在后代的胎儿和成人肝脏中分析了基因表达和DNA甲基化.

主要成果:

从PE怀孕后的后代表现出体重增加,肝脏脂质积累,脂肪细胞扩大和能量平衡受损,持续到成年.
RNA测序揭示了PE后代肝脏中参与脂质代谢的基因 (例如Gpat3,Cpt1a) 的改变表达.
激光测序确定了Gpat3和Cpt1a中的促进物低甲基化和高甲基化,与改变的基因表达相关,表明从胎儿到成年阶段的持续表观遗传变化.

结论:

研究结果表明,甲基化介导的表观遗传机制驱动PE怀孕后代的代际脂质积累和代谢功能障碍.
这些表观遗传变化有助于能量平衡受损和肥胖,增加了晚年对代谢障碍的易感性.
对暴露于母体PE的后代进行早期干预,可能有助于降低他们患代谢障碍的风险.

关键词:

通过DNA甲基化.代际遗传是一种世代间的遗传.脂质新陈代谢脂质新陈代谢代谢障碍是一种代谢障碍.孕产妇产前炎症孕产妇产前炎症

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