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イデノ ヒサシ
Ideno Hisashi
出野 尚 所属 鶴見大学 歯学部 歯学科 薬理学 職種 講師 |
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| 論文種別 | 【査読あり】 研究論文（学術雑誌） |
| 言語種別 | 英語 |
| 査読の有無 | 査読あり |
| 表題 | G9a is involved in the regulation of cranial bone formation through activation of Runx2 function during development. |
| 掲載誌名 | 正式名：Bone |
| 巻・号・頁 | 137,pp.115332-115332 |
| 著者・共著者 | Hisashi Ideno,Kazuhisa Nakashima,Koichiro Komatsu,Ryoko Araki,Masumi Abe,Yoshinori Arai,Hiroshi Kimura,Yoichi Shinkai,Makoto Tachibana,Akira Nifuji |
| 発行年月 | 2020/04 |
| 概要 | The methyltransferase G9a was originally isolated as a histone methyltransferase that catalyzes the methylation of histone 3 lysine 9 (H3K9) to a dimethylated state (H3K9me2). Recent studies have revealed that G9a has multiple functions in various cells, including osteoblasts. Here, we investigated G9a function during cranial bone formation. Crossing Sox9-cre with G9aflox/flox (fl/fl) mice generated conditional knockout mice lacking G9a expression in Sox9-positive neural crest-derived bone cells. Sox9-Cre/G9afl/fl mice showed severe hypo-mineralization of cranial vault bones, including defects in nasal, frontal, and parietal bones with opened fontanelles. Cell proliferation was inhibited in G9a-deleted calvarial bone tissues. Expression levels of bone marker genes, i.e., alkaline phosphatase and osteocalcin, were suppressed, whereas Runx2 expression was not significantly decreased in those tissues. In vitro experiments using G9a-deleted calvarial osteoblasts showed decreased cell proliferation after G9a deletion. In G9a-deleted osteoblasts, expression levels of fibroblast growth factor receptors and several cyclins were suppressed. Moreover, the expression of bone marker genes was |
| DOI | 10.1016/j.bone.2020.115332 |
| PMID | 32344102 |