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首页> 外文期刊>Cell and Tissue Research >Epigenetic regulation of Tbx18 gene expression during endochondral bone formation
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Epigenetic regulation of Tbx18 gene expression during endochondral bone formation

机译：软骨内骨形成过程中Tbx18基因表达的表观遗传调控

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摘要

Endochondral bone formation is tightly regulated by the spatial and sequential expression of a series of transcription factors. To disclose the roles of TBX18, a member of the T-box transcription factor family, during endochondral bone formation, its spatial and temporal expression patterns were characterized in the limb skeletal region of the developing mouse together with those of established osteochondrogenic markers Sox9, Col2a1, and Runx2. TBX18 expression first appeared in condensed mesenchymal cells (chondro-progenitors) in embryonic-day-10.5 (E10.5) limb bud and was co-localized with Sox9 expression, whereas at E11.5 and E12.5, it became undetectable in mesenchymal cells committed to the chondrocyte lineage. From E13.5 to E18.5, TBX18 expression reappeared in chondrocytes, correlating strongly with Col2a1 expression; furthermore, low level TBX18 expression was found in the Runx2-positive perichondral osteoblastic cell lineage. At the postnatal stage, TBX18 expression was observed in epiphyseal chondrocytes and osteocytes within the lacunae of mature trabecular bone. On the assumption that such characteristic Tbx18 gene expression is epigenetically regulated during mouse limb development, we examined the methylation status of the CpG-island in the mouse Tbx18 gene by methylation-specific polymerase chain reaction. Hypermethylation of the Tbx18 gene promoter became evident at an early embryonic stage in TBX18-negative cells and then disappeared at a late embryonic stage in TBX18-positive cells. Therefore, the temporal suppression of Tbx18 gene expression by the hypermethylation of its promoter seems to trigger the differentiation of mesenchymal cells into hypertrophic chondrocytes in the early stages of endochondral ossification.
机译：一系列转录因子的空间表达和顺序表达严格控制着软骨内骨的形成。为了揭示T-box转录因子家族成员TBX18在软骨内骨形成过程中的作用，其时空表达模式在发育中小鼠的肢体骨骼区域以及已建立的骨软骨生成标记物Sox9，Col2a1进行了表征。和Runx2。 TBX18表达首先出现在胚胎天10.5（E10.5）肢芽的浓缩间充质细胞（软骨祖细胞）中，并与Sox9表达共定位，而在E11.5和E12.5时，它在间充质中无法检测到细胞定型为软骨细胞谱系。从E13.5到E18.5，TBX18表达重新出现在软骨细胞中，与Col2a1表达密切相关。此外，在Runx2阳性软骨周围成骨细胞谱系中发现了低水平的TBX18表达。在产后阶段，在成熟的小梁骨腔内骨cho软骨细胞和骨细胞中观察到了TBX18表达。假设这种特征性Tbx18基因表达在小鼠肢体发育过程中受到表观遗传调控，我们通过甲基化特异性聚合酶链反应检查了小鼠Tbx18基因中CpG岛的甲基化状态。 Tbx18基因启动子的高甲基化在TBX18阴性细胞的胚胎早期阶段就很明显，然后在TBX18阳性细胞的胚胎后期阶段就消失了。因此，Tbx18基因表达的启动子过度甲基化在时间上的抑制似乎在软骨内骨化的早期触发了间充质细胞向肥大软骨细胞的分化。

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