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母体高脂肪饮食改变了骨组织中的表观遗传标记 H3K27me3 和 H3K27ac,从而调节了小鼠后代成骨细胞的生成。

Maternal high-fat diet modifies epigenetic marks H3K27me3 and H3K27ac in bone to regulate offspring osteoblastogenesis in mice.

机构信息

Arkansas Children's Nutrition Center Little Rock, AR 72202, USA.

Department of Pediatrics, University of Arkansas for Medical Sciences, Little Rock, AR, USA.

出版信息

Epigenetics. 2022 Dec;17(13):2209-2222. doi: 10.1080/15592294.2022.2111759. Epub 2022 Aug 17.

Abstract

Studies from both humans and animal models indicated that maternal chronic poor-quality diet, especially a high fat diet (HFD), is significantly associated with reduced bone density and childhood fractures in offspring. When previously studied in a rat model, our data suggested that maternal HFD changes epigenetic marks such as DNA methylation and histone modifications to control osteoblast metabolism. In mouse embryonic and postnatal offspring bone samples, a ChIP-sequencing (ChIP-Seq)-based genome-wide method was used to locate the repressive histone mark H3K27me3 (mediated via the polycomb histone methyltransferase, ) and expressive histone mark H3K27ac ( mediated) throughout the genome. Using isolated mouse embryonic cells from foetal calvaria (osteoblast-like cells), H3K27me3 ChIP-Seq showed that 147 gene bodies and 26 gene promoters in HFD embryotic samples had a greater than twofold increase in H3K27me peaks compared to controls. Among the HFD samples, and that are important genes playing roles during chondro- and osteogenesis had significantly enriched levels of H3K27me3. Their decreased mRNA expression was confirmed by real-time PCR and standard ChIP analysis, indicating a strong association with mediated H3K27me3 epigenetic changes. Using embryonic calvaria osteoblastic cells and offspring bone samples, H3K27ac ChIP-Seq analysis showed that osteoblast inhibitor genes and had significantly enriched peaks of H3K27ac in HFD samples compared to controls. Their increased gene expression and association with H3K27ac were also confirmed by real-time PCR and standard ChIP analysis. These findings indicate that chronic maternal HFD changes histone trimethylation and acetylation epigenetic marks to regulate expression of genes controlling osteoblastogenesis.

摘要

来自人类和动物模型的研究表明,母体慢性低质量饮食,尤其是高脂肪饮食(HFD),与后代骨密度降低和儿童骨折显著相关。当在大鼠模型中进行先前研究时,我们的数据表明,母体 HFD 会改变表观遗传标记,如 DNA 甲基化和组蛋白修饰,以控制成骨细胞代谢。在小鼠胚胎和产后后代骨样本中,使用基于染色质免疫沉淀测序(ChIP-Seq)的全基因组方法来定位抑制性组蛋白标记 H3K27me3(通过多梳组蛋白甲基转移酶介导)和表达性组蛋白标记 H3K27ac(通过介导)在整个基因组中。使用来自胎儿颅骨的分离的小鼠胚胎细胞(成骨样细胞),H3K27me3 ChIP-Seq 显示,与对照相比,HFD 胚胎样本中有 147 个基因体和 26 个基因启动子的 H3K27me 峰增加了两倍以上。在 HFD 样本中,在软骨和成骨过程中发挥重要作用的 和 等重要基因具有明显富集的 H3K27me3。通过实时 PCR 和标准 ChIP 分析证实了它们的 mRNA 表达降低,表明与 介导的 H3K27me3 表观遗传变化有很强的关联。使用胚胎颅骨成骨细胞和后代骨样本,H3K27ac ChIP-Seq 分析表明,与对照相比,HFD 样本中骨细胞抑制剂基因 和 具有明显富集的 H3K27ac 峰。通过实时 PCR 和标准 ChIP 分析也证实了它们的基因表达增加和与 H3K27ac 的关联。这些发现表明,慢性母体 HFD 改变组蛋白三甲基化和乙酰化表观遗传标记,以调节控制成骨细胞发生的基因表达。

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