論文

国際誌
2020年

Establishment of bone marrow-derived M-CSF receptor-dependent self-renewing macrophages.

Cell death discovery
  • Hesham Nasser
  • ,
  • Partho Adhikary
  • ,
  • Amira Abdel-Daim
  • ,
  • Osamu Noyori
  • ,
  • Jutatip Panaampon
  • ,
  • Ryusho Kariya
  • ,
  • Seiji Okada
  • ,
  • Wenjuan Ma
  • ,
  • Masaya Baba
  • ,
  • Hitoshi Takizawa
  • ,
  • Mariko Yamane
  • ,
  • Hitoshi Niwa
  • ,
  • Shinya Suzu

6
開始ページ
63
終了ページ
63
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1038/s41420-020-00300-3

Recent studies have revealed that tissue macrophages are derived from yolk sac precursors or fetal liver monocytes, in addition to bone marrow monocytes. The relative contribution of these cells to the tissue macrophage pool is not fully understood, but embryo-derived cells are supposed to be more important because of their capacity to self-renew. Here, we show the presence of adult bone marrow-derived macrophages that retain self-renewing capacity. The self-renewing macrophages were readily obtained by long-term culture of mouse bone marrow cells with macrophage colony-stimulating factor (M-CSF), a key cytokine for macrophage development. They were non-tumorigenic and proliferated in the presence of M-CSF in unlimited numbers. Despite several differences from non-proliferating macrophages, they retained many features of cells of the monocytic lineage, including the differentiation into dendritic cells or osteoclasts. Among the transcription factors involved in the self-renewal of embryonic stem cells, Krüppel-like factor 2 (KLF2) was strongly upregulated upon M-CSF stimulation in the self-renewing macrophages, which was accompanied by the downregulation of MafB, a transcription factor that suppresses KLF2 expression. Indeed, knockdown of KLF2 led to cell cycle arrest and diminished cell proliferation in the self-renewing macrophages. Our new cell model would be useful to unravel differences in phenotype, function, and molecular mechanism of proliferation among self-renewing macrophages with different origins.

リンク情報
DOI
https://doi.org/10.1038/s41420-020-00300-3
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/32714570
PubMed Central
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7378060
ID情報
  • DOI : 10.1038/s41420-020-00300-3
  • PubMed ID : 32714570
  • PubMed Central 記事ID : PMC7378060

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