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ナカシマ カズヒサ
Nakashima Kazuhisa
中島 和久 所属 鶴見大学 歯学部 歯学科 薬理学 職種 准教授 |
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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 | PIASx beta is a key regulator of osterix transcriptional activity and matrix mineralization in osteoblasts |
| 掲載誌名 | 正式名：JOURNAL OF CELL SCIENCE ISSNコード：00219533 |
| 出版社 | COMPANY OF BIOLOGISTS LTD |
| 巻・号・頁 | 120(15),pp.2565-2573 |
| 著者・共著者 | Md. Moksed Ali,Tatsuya Yoshizawa,Osamu Ishibashi,Akio Matsuda,Junko Shimomura,Hisashi Mera,Kazuhisa Nakashima,Hiroyuki Kawashima |
| 発行年月 | 2007/08 |
| 概要 | We recently reported that tensile stress induces osteoblast differentiation and osteogenesis in the mouse calvarial suture in vitro. Using this experimental system, we identified PIASx beta, a splice isoform of Pias2, as one of the genes most highly upregulated by tensile stress. Further study using cell culture revealed that this upregulation was transient and was accompanied by upregulation of other differentiation markers, including osterix, whereas expression of Runx2 was unaffected. Runx2 and osterix are the two master proteins controlling osteoblast differentiation, with Runx2 being upstream of osterix. Targeted knockdown of PIASx beta by small interfering RNA (siRNA) markedly suppressed osteoblastic differentiation and matrix mineralization, whereas transient overexpression of PIASx beta caused the exact opposite effects. Regardless of PIASx beta expression level, Runx2 expression remained constant. Reporter assays demonstrated that osterix enhanced its own promoter activity, which was further stimulated by PIASx beta but not by its sumoylation-defective mutant. NFATc1 and NFATc3 additionally increased osterix transcriptional activity when co-transfected with PIASx beta. Bec |
| DOI | 10.1242/jcs.005090 |
| PMID | 17623776 |