Understanding the factors that regulate hematopoiesis opens up the possibility of modifying these factors and their actions for clinical benefit. DEK, a non-histone nuclear phosphoprotein initially identified as a putative proto-oncogene, has recently been linked to regulate hematopoiesis. DEK has myelosuppressive activity in vitro on proliferation of human and mouse hematopoietic progenitor cells and enhancing activity on engraftment of long-term marrow repopulating mouse stem cells, has been linked in coordinate regulation with the transcription factor C/EBPα, for differentiation of myeloid cells, and apparently targets a long-term repopulating hematopoietic stem cell for leukemic transformation. This review covers the uniqueness of DEK, what is known about how it now functions as a nuclear protein and also as a secreted molecule that can act in paracrine fashion, and how it may be regulated in part by dipeptidylpeptidase 4, an enzyme known to truncate and modify a number of proteins involved in activities on hematopoietic cells. Examples are provided of possible future areas of investigation needed to better understand how DEK may be regulated and function as a regulator of hematopoiesis, information possibly translatable to other normal and diseased immature cell systems.
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http://dx.doi.org/10.1002/stem.1443 | DOI Listing |
J Transl Autoimmun
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Rheumatology Research Center, Tehran University of Medical Science, Tehran, Iran.
Iron is a crucial element for living organism in terms of oxygen transport, hematopoiesis, enzymatic activity, mitochondrial respiratory chain function and also immune system function. The human being has evolved a mechanism to regulate body iron. In some rheumatic diseases such as rheumatoid arthritis (RA), systemic lupus erythematous (SLE), systemic sclerosis (SSc), ankylosing spondylitis (AS), and gout, this balanced iron regulation is impaired.
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January 2025
Division of Cell Regulation, Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan; Division of Cell Engineering, Center for Stem Cell Biology and Regenerative Medicine, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan; Laboratory for Stem Cell Therapy, Faculty of Medicine, Tsukuba University, Ibaraki, Japan. Electronic address:
Hematopoietic stem cells (HSCs) possess the capacity to regenerate the entire hematopoietic system. However, the precise HSC dynamics in the early post-transplantation phase remain an enigma. Clinically, the initial hematopoiesis in the post-transplantation period is critical, necessitating strategies to accelerate hematopoietic recovery.
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January 2025
Research Center for High Altitude Medicine, Qinghai University, Xining 810016, China.
The hypoxia-inducible factor (HIF) pathway has been demonstrated to play a pivotal role in the process of high-altitude adaptation. PHD2, a key regulator of the HIF pathway, has been found to be associated with erythropoiesis. However, the relationship between changes in Phd2 abundance and erythroid differentiation under hypoxic conditions remains to be elucidated.
View Article and Find Full Text PDFBiology (Basel)
January 2025
Department of Hematology, the Second Xiangya Hospital, School of Life Sciences, Hunan Province Key Laboratory of Basic and Applied Hematology, Central South University, Changsha 410011, China.
B-cell lymphoma/leukemia 11A (BCL11A) is a crucial transcriptional regulator, widely recognized for its role in controlling fetal hemoglobin and its potential as a gene therapy target for inherited hemoglobinopathies. Beyond this, recent studies have also highlighted its key role in the maturation and function of immune cells and erythrocytes, mediated through the regulation of various molecules during hematopoietic development. The dysregulation of BCL11A disrupts downstream molecular pathways, contributing to the development of several hematological malignancies, particularly leukemias.
View Article and Find Full Text PDFJ Exp Med
March 2025
Division of Innate Immunity, The Institute of Medical Science, The University of Tokyo, Minato-ku, Japan.
Lysosomal stress due to the accumulation of nucleic acids (NAs) activates endosomal TLRs in macrophages. Here, we show that lysosomal RNA stress, caused by the lack of RNase T2, induces macrophage accumulation in multiple organs such as the spleen and liver through TLR13 activation by microbiota-derived ribosomal RNAs. TLR13 triggered emergency myelopoiesis, increasing the number of myeloid progenitors in the bone marrow and spleen.
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