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大胎龄新生儿造血干细胞静止信号的表观遗传和转录组编程。

Epigenetic and Transcriptomic Programming of HSC Quiescence Signaling in Large for Gestational Age Neonates.

机构信息

Inserm U1283, CNRS UMR 8199, European Genomic Institute for Diabetes, Institut Pasteur de Lille, 59000 Lille, France.

Lille University Hospital, University of Lille, 59000 Lille, France.

出版信息

Int J Mol Sci. 2022 Jun 30;23(13):7323. doi: 10.3390/ijms23137323.

DOI:10.3390/ijms23137323
PMID:35806330
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9267056/
Abstract

Excessive fetal growth is associated with DNA methylation alterations in human hematopoietic stem and progenitor cells (HSPC), but their functional impact remains elusive. We implemented an integrative analysis combining single-cell epigenomics, single-cell transcriptomics, and in vitro analyses to functionally link DNA methylation changes to putative alterations of HSPC functions. We showed in hematopoietic stem cells (HSC) from large for gestational age neonates that both DNA hypermethylation and chromatin rearrangements target a specific network of transcription factors known to sustain stem cell quiescence. In parallel, we found a decreased expression of key genes regulating HSC differentiation including , and . Our functional analyses showed that this epigenetic programming was associated with a decreased ability for HSCs to remain quiescent. Taken together, our multimodal approach using single-cell (epi)genomics showed that human fetal overgrowth affects hematopoietic stem cells' quiescence signaling via epigenetic programming.

摘要

胎儿过度生长与人类造血干/祖细胞（HSPC）中的 DNA 甲基化改变有关，但它们的功能影响仍不清楚。我们实施了一项综合分析，结合单细胞表观基因组学、单细胞转录组学和体外分析，将 DNA 甲基化变化与 HSPC 功能的潜在改变联系起来。我们在来自巨大儿的造血干细胞（HSC）中表明，DNA 过度甲基化和染色质重排都针对一个已知维持干细胞静止的特定转录因子网络。同时，我们发现调节 HSC 分化的关键基因的表达水平降低，包括 、 和 。我们的功能分析表明，这种表观遗传编程与 HSCs 保持静止的能力下降有关。总之，我们使用单细胞（表观）基因组学的多模态方法表明，人类胎儿过度生长通过表观遗传编程影响造血干细胞的静止信号。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74a3/9267056/cae892614e76/ijms-23-07323-g007.jpg
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