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CHD7通过甲状旁腺激素1型受体（PTH1R）信号通路调控人牙囊细胞的成骨分化。

CHD7 Regulates Osteogenic Differentiation of Human Dental Follicle Cells via PTH1R Signaling.

作者信息

Liu Caojie, Li Qiwen, Xiao Qingyue, Gong Ping, Kang Ning

机构信息

West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan Province, China.

出版信息

Stem Cells Int. 2020 Sep 21;2020:8882857. doi: 10.1155/2020/8882857. eCollection 2020.

DOI:10.1155/2020/8882857
PMID:33014071
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7525296/
Abstract

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 impairs the osteogenic ability of hDFCs, characterized by reduced alkaline phosphatase activity and mineralization, and the decreased expression of osteogenesis-related genes. Conversely, the 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 knockdown. We found the expression of PTH1R positively correlates with CHD7. Importantly, the overexpression of in -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.

摘要

染色质结构域解旋酶DNA结合蛋白7（CHD7）是一种依赖ATP的染色质重塑酶，作为染色质阅读器发挥作用以进行表观遗传修饰。其对人牙囊细胞（hDFCs）成骨分化的影响尚不清楚。在此，我们表明CHD7表达随着成骨分化而增加。CHD7的敲低会损害hDFCs的成骨能力，其特征是碱性磷酸酶活性和矿化减少，以及成骨相关基因的表达降低。相反，CHD7的过表达增强了hDFCs的成骨分化。在机制上，RNA测序分析显示CHD7敲低后甲状旁腺激素（PTH）/甲状旁腺激素受体-1（PTH1R）信号通路的富集下调。我们发现PTH1R的表达与CHD7呈正相关。重要的是，在CHD7敲低的hDFCs中过表达PTH1R可部分挽救受损的成骨分化。我们的研究表明，CHD7通过调节PTH1R的转录来调节hDFCs的成骨分化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa85/7525296/61f589a28916/SCI2020-8882857.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa85/7525296/20c74e1a4980/SCI2020-8882857.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa85/7525296/73b88f1298cb/SCI2020-8882857.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa85/7525296/054075989d18/SCI2020-8882857.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa85/7525296/07981337290b/SCI2020-8882857.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa85/7525296/e3b456da6084/SCI2020-8882857.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa85/7525296/61f589a28916/SCI2020-8882857.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa85/7525296/20c74e1a4980/SCI2020-8882857.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa85/7525296/73b88f1298cb/SCI2020-8882857.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa85/7525296/054075989d18/SCI2020-8882857.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa85/7525296/07981337290b/SCI2020-8882857.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa85/7525296/e3b456da6084/SCI2020-8882857.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa85/7525296/61f589a28916/SCI2020-8882857.006.jpg

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