If you store books on a bookshelf, tools in a toolbox, and a broom in a broom closet at home, you can easily reach these items when you need them. In the body, hematopoietic stem cells (HSCs) reside on their own specialized “spots” in the bone marrow, known as HSC niches. Recently, researchers in Japan have identified genes that play key roles within these niches.
In a new study published in nature communication, researchers led by Osaka University have shed new light on the role of transcription factors Runx1 and Runx2 in bone marrow microenvironments known as HSC niches. HSC niches are essential for the maintenance of HSCs, from which blood cells are formed.
An important component of HSC niches is a cell type known as CXC chemokine ligand 12-abundant reticular (CAR) cells. CAR cells express signaling molecules known as cytokines that are important for the maintenance of hematopoietic stem and progenitor cells (HSPCs). The team previously found that CAR cells express a transcription factor called Runx2, which is known to play a role in skeletal development. In this study, they recently discovered that CAR cells also express Runx1, which is known to be essential for hematopoietic stem cell development. However, it is completely unknown how Runx transcription factors function in maintaining HSC niches, which prompted the research team to investigate this role.
“To evaluate the impact of Runx transcription factors on bone marrow, we used mouse models in which Runx1 and/or Runx2 were specifically deleted in CAR cells,” said lead author Yoshiki Omatsu.
The researchers found that mice without Runx1 in mesenchymal cells, including CAR cells, showed normal bone and bone marrow development, while mice without Runx2 showed normal CAR cells and bone marrow, but short and immature bone. However, mice lacking both Runx1 and Runx2 in CAR cells showed a significant reduction in HSPCs and immune cells, along with an increase in fibrosis (the abnormal build-up of connective tissue) in the bone marrow, a hallmark of a condition known as myelofibrosis. †
“Our results strongly point to the essential role of Runx1 and/or Runx2 in the inhibition of fibrosis and maintenance of the HSC niche,” said senior author Takashi Nagasawa.
The research team also found that in a mouse model of primary myelofibrosis, the expression of Runx1 and Runx2 was reduced, while the expression of fibrotic genes was increased, further highlighting the role of Runx1 and Runx2 in the inhibition of fibrosis in the bone marrow. While more work is needed on this topic, these findings suggest that Runx1 and Runx2 may be potential targets for the diagnosis and treatment of myelofibrosis.
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