論文

査読有り
2017年12月

Effects of in vivo deletion of GATA2 in bone marrow stromal cells

EXPERIMENTAL HEMATOLOGY
  • Shin Hasegawa
  • ,
  • Tohru Fujiwara
  • ,
  • Yoko Okitsu
  • ,
  • Hiroki Kato
  • ,
  • Yuki Sato
  • ,
  • Noriko Fukuhara
  • ,
  • Yasushi Onishi
  • ,
  • Ritsuko Shimizu
  • ,
  • Masayuki Yamamoto
  • ,
  • Hideo Harigae

56
開始ページ
31
終了ページ
45
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.exphem.2017.08.004
出版者・発行元
ELSEVIER SCIENCE INC

The bone marrow (BM) microenvironment comprises multiple stem cell niches derived from BM mesenchymal stem cells (MSCs). Previous in vitro analyses have suggested that transcription factor GATA2 plays an important role in adipocyte differentiation of BM-MSCs and in hematopoietic support, but the role of GATA2 in vivo remains unknown. We evaluated GATA2 effects in BM-MSCs in vivo. Expression profiling analysis of Gata2-knockout Ter119(-)CD45(-) mesenchymal stromal cells obtained from compact bone from tamoxifen-treated Gata2 conditional knockout mice (Gata2(f/f)/ER-Cre mice) revealed upregulation of 110 genes and downregulation of 141 genes by a factor of 2. Moreover, gene ontology analysis revealed significant enrichment of genes involved in cell adhesion and chemotaxis. We did not find any phenotypic changes when Gata2 was deleted with BM-MSC-related gene promoters, such as Nestin, Prx1, and Lepr, except for a significant decrease in the colony number of Gata2(f/f)/Prx1-Cre mice. There was a significant decrease in the percentage of the common myeloid progenitor fraction when Gata2 was deleted in all BM cells, except hematopoietic cells after normal BM cells were transplanted into irradiated Gata2(f/f)/ER-Cre mice with Gata2 subsequently knocked out by tamoxifen administration. In conclusion, GATA2 could affect the function of BMMSCs in vivo, presumably by regulating the expression of extracellular signals. (C) 2017 ISEH - Society for Hematology and Stem Cells. Published by Elsevier Inc. All rights reserved.

リンク情報
DOI
https://doi.org/10.1016/j.exphem.2017.08.004
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000416614100004&DestApp=WOS_CPL
ID情報
  • DOI : 10.1016/j.exphem.2017.08.004
  • ISSN : 0301-472X
  • eISSN : 1873-2399
  • Web of Science ID : WOS:000416614100004

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