Scholarlink

<p>MAFB, a transcription factor of the large Maf family, is expressed in both fetal liver (FL) and bone marrow (BM) hematopoietic stem cells (HSCs). However, its stage-specific roles remain elusive. Here, we reveal that MAFB plays distinct roles in FL and BM HSCs. Using <i>Mafb</i>-deficient and <i>Mafb</i>-GFP knock-in mouse models, we demonstrate that <i>Mafb</i> deletion enhances proliferation, cell cycle entry, and myeloid differentiation of FL HSCs, leading to enhanced chimerism rate in transplantation assays. However, <i>Mafb</i>-deficient BM HSCs exhibit impaired long-term reconstitution and progressive exhaustion, supported by serial transplantation and reduced colony-forming capacity. HSCs from <i>Mafb</i><sup>f/f</sup>::<i>Tie2</i>-Cre mouse (<i>Mafb</i> cKO) further revealed a significant decline in long-term HSC (LT-HSC) populations and multilineage differentiation potential. Together, our findings suggest a stage-dependent role of MAFB as a regulator of HSC proliferation during fetal development and a critical factor for HSC maintenance during adulthood, providing insights into the stage-specific regulation of HSC function linked to cell cycle control and long-term repopulation capacity.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

MAFB regulates hematopoietic stem cell proliferation and maintenance

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年11月18日

查看全文
  • Saki Asano,
  • Ching-Wei Liao,
  • Yurina Matsunaga,
  • Hyojung Jeon,
  • Kyoko Sawaguchi,
  • Keigo Asano,
  • Manabu Kusakabe,
  • Zeynab Javanfekr Shahri,
  • Natalia Gogoleva,
  • Tomomasa Yokomizo,
  • Satoru Takahashi,
  • Michito Hamada

摘要

MAFB, a transcription factor of the large Maf family, is expressed in both fetal liver (FL) and bone marrow (BM) hematopoietic stem cells (HSCs). However, its stage-specific roles remain elusive. Here, we reveal that MAFB plays distinct roles in FL and BM HSCs. Using Mafb-deficient and Mafb-GFP knock-in mouse models, we demonstrate that Mafb deletion enhances proliferation, cell cycle entry, and myeloid differentiation of FL HSCs, leading to enhanced chimerism rate in transplantation assays. However, Mafb-deficient BM HSCs exhibit impaired long-term reconstitution and progressive exhaustion, supported by serial transplantation and reduced colony-forming capacity. HSCs from Mafbf/f::Tie2-Cre mouse (Mafb cKO) further revealed a significant decline in long-term HSC (LT-HSC) populations and multilineage differentiation potential. Together, our findings suggest a stage-dependent role of MAFB as a regulator of HSC proliferation during fetal development and a critical factor for HSC maintenance during adulthood, providing insights into the stage-specific regulation of HSC function linked to cell cycle control and long-term repopulation capacity.