PubMed · 71885
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
L Kass. 1977. A note on reticulocytes.. https://pubmed.ncbi.nlm.nih.gov/71885/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
INTRODUCTION: The pathogenesis of anemia and other erythroid dysphasia are mains poorly understood, primarily due to limited knowledge about the differentiation processes and regulatory mechanisms governing erythropoiesis. Erythropoiesis is a highly complex and precise biological process, that can be categorized into three distinct stages: early erythropoiesis, terminal erythroid differentiation, and reticulocyte maturation, and this complex process is tightly controlled by multiple regulatory factors. Emerging evidence highlights the crucial role of epigenetic modifications, particularly histone modifications, in regulating erythropoiesis. Methylation and acetylation are two common modification forms that affect genome accessibility by altering the state of chromatin, thereby regulating gene expression during erythropoiesis. DISCUSSION: This review systematically examines the roles of histone methylation and acetylation, along with their respective regulatory enzymes, in regulating the development and differentiation of hematopoietic stem/progenitor cells (HSPCs) and erythroid progenitors. Furthermore, we discuss the involvement of these histone modifications in erythroid-specific developmental processes, including hemoglobin switching, chromatin condensation, and enucleation.Conclusions This review summarizes the current understanding of the role of histone modifications in erythropoiesis based on existing research, as a foundation for further research the mechanisms of epigenetic regulatory in erythropoiesis.
Explore the source record for details and available documents.
Regulation of erythropoiesis by erythropoietin, proposed already at the beginning of this century, has been greatly enhanced by cloning and expression of the gene of erythropoietin. Erythropoietin gene functions as a housekeeping gene, so that erythropoietin is constitutively produced and is never absent from the blood. Hypoxia activates erythropoietin gene primarily in the kidney and also to a small extent in the liver. Peritubular interstitial cells in the kidney or the kidney tubular cells produce erythropoietin. The modulation of erythropoietin gene expression in the kidney and the liver differs. Kidney cells produce erythropoietin in all-or-non pattern and as the stimulus becomes more severe more cells produce erythropoietin while in the liver individual cells produce more erythropoietin when the stimulus is more severe. Erythropoietin exerts its effect on erythroid progenitor cells after binding to specific receptors that are expressed on target cells, interacts with those cells in the bone marrow stimulating them into cell cycle, supporting the survival of cycling progenitor cells and permitting their final differentiation into cells synthetizing hemoglobin.