Erythroid cells derive from pluripotent hematopoietic stem cells at the embryonic, fetal, and adult stages of hematopoiesis. The process of erythropoiesis is driven by cis- and trans-regulatory elements that operate together to mediate expression of developmental- and differentiation-stage specific activities ...
Erythroid cells derive from pluripotent hematopoietic stem cells at the embryonic, fetal, and adult stages of hematopoiesis. The process of erythropoiesis is driven by cis- and trans-regulatory elements that operate together to mediate expression of developmental- and differentiation-stage specific activities ultimately leading to the formation of red blood cells (RBCs). Adult humans contain 10 to 20 trillion RBCs, and each second 2.5 million RBCs are released into the blood stream. The lifetime of RBCs is about 120 days, after which they are removed by macrophages residing primarily in the spleen. The formation of RBCs involves successive steps of cell division and differentiation from hematopoietic progenitor cells, a process stimulated by the hormone erythropoietin. The progression to mature erythroid cells involves expression of transcription factors and non-coding RNA that guide cells to differentiate along the erythroid lineage. During the final stages of RBC maturation, the chromatin condenses and the nucleus is eventually evicted. Among the master regulators of erythropoiesis are GATA transcription factors 1 and 2, erythroid krüpple like factor 1 (KLF1), and Tal1, which forms a protein complex with GATA factors and the co-regulator LMO2. Erythroid cells are specialized for the gas transport and express extremely high levels of hemoglobin. In addition, erythroid cells contain a characteristic cell membrane that confers flexibility and provides protection from shear-stress during the flow of RBCs through tiny blood vessels. Mutations in globin genes or genes encoding red blood cell membrane proteins cause anemias, due to deficiency of RBC formation and/or function.
Understanding molecular mechanisms involved in erythropoiesis will guide novel therapies for anemias, which are among the most common genetic diseases in the human population. Recent advances in single cell technologies has advanced our understanding of erythropoiesis but challenges remain. Likewise, current gene therapy or gene editing trials are promising but also highlight areas that need to be improved.
We invite submissions of research articles as well as reviews and mini-reviews. Below are examples of topics included:
- Role of transcription factors and non-coding RNA in erythropoiesis.
- Regulation of the α- and ß-globin gene loci.
- Role of the embryonic yolk sac, fetal liver, and bone marrow microenvironment in erythropoiesis.
- Advances in understanding erythropoiesis through single-cell RNA and ATAC sequencing.
- Erythropoiesis and metabolomics.
- Diamond Blackfan Anemia.
- Formation of the erythroid cell membrane.
- Epo-signaling and the role of other cytokines and growth factors in the formation of RBCs.
- Nuclear eviction during final stages of erythroid maturation.
- Molecular mechanisms causing anemias and therapeutic strategies.
Keywords:
Globin genes, Transcription Factor, Non-coding RNA, Red Blood Cell, Red Blood Cell Membrane, Hematopoiesis, Erythropoiesis, Reticulocyte, Bone marrow, Anemia
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.