Chromodomain helicase DNA-binding protein 7 (CHD7) is an ATP-dependent chromatin remodeling enzyme, functioning as chromatin reader to conduct epigenetic modification. Its effect on osteogenic differentiation of human dental follicle cells (hDFCs) remains unclear. Here, we show the CHD7 expression increases with osteogenic differentiation. The knockdown of CHD7 impairs the osteogenic ability of hDFCs, characterized by reduced alkaline phosphatase activity and mineralization, and the decreased expression of osteogenesis-related genes. Conversely, the CHD7 overexpression enhances the osteogenic differentiation of hDFCs. Mechanically, RNA-seq analyses revealed the downregulated enrichment of PTH (parathyroid hormone)/PTH1R (parathyroid hormone receptor-1) signaling pathway after CHD7 knockdown. We found the expression of PTH1R positively correlates with CHD7. Importantly, the overexpression of PTH1R in CHD7-knockdown hDFCs partially rescued the impaired osteogenic differentiation. Our research demonstrates that CHD7 regulates the osteogenic differentiation of hDFCs by regulating the transcription of PTH1R.

中文翻译：

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CHD7通过PTH1R信号调节人牙囊细胞的成骨分化

染色体域解旋酶DNA结合蛋白7（CHD7）是ATP依赖的染色质重塑酶，可作为染色质读取器进行表观遗传修饰。它对人牙囊细胞（hDFCs）成骨分化的影响尚不清楚。在这里，我们显示CHD7表达随成骨分化而增加。敲低CHD7会损害hDFC的成骨能力，其特征是碱性磷酸酶活性和矿化度降低，以及成骨相关基因的表达降低。相反，CHD7的过表达增强了hDFC的成骨分化。机械上，RNA-seq分析显示，PTH（甲状旁腺激素）/ PTH1R（甲状旁腺激素受体-1）信号通路的富集在下调后CHD7组合式。我们发现PTH1R的表达与CHD7正相关。重要的是，在CHD7基因敲低的hDFC中PTH1R的过度表达部分挽救了成骨分化受损。我们的研究表明，CHD7通过调节PTH1R的转录来调节hDFC的成骨分化。