Health
Discovery of a new method for controlling erythropoiesis
Red blood cells are the most abundant cells in the body. It has long been known that when red blood cells are destroyed or bleeding causes anemia, the hormone erythropoietin (EPO) increases and causes immature cells (erythroblasts) to proliferate and eventually become red blood cells, restoring red blood cell counts. However, little was known about how more primitive “hematopoietic stem cells” respond to severe anemia. Hematopoietic stem cells have the capacity to generate all types of blood cells, but because they lack receptors for erythropoietin, an unknown mechanism must help restore red blood cell counts.
To investigate this, the research team induced acute anemia in mice by using a drug that destroys red blood cells (phenylhydrazine) or by drawing blood (phlebotomy), and then analyzed changes in hematopoietic stem cells in the bone marrow to explore how these changes were induced.
They found that when acute anemia was induced, hematopoietic stem cells immediately began to proliferate. In addition, hematopoietic stem cells in anemic mice produced more red blood cells than other blood cells, a response not seen in normal mice. Because hematopoietic stem cells do not respond to erythropoietin, the researchers performed genetic analysis to elucidate the cause of the changes in hematopoietic stem cells. As a result, they found that genes involved in lipid metabolism were activated immediately after the onset of anemia, and in particular the function of the very low density lipoprotein receptor (VLDL receptor, VLDLR) was increased.
In this study, hematopoietic stem cells were classified into two types: those with high VLDLR expression (VLDLRexpensive Hematopoietic stem cells) and cells with low VLDLR expression (VLDLRlow Hematopoietic stem cells).expensive Hematopoietic stem cells were more likely to produce red blood cells. Analysis of lipids and associated proteins in the bone marrow of anemic mice showed that VLDL levels were reduced, but apolipoprotein E (ApoE), a component of VLDL, rapidly increased. In genetically modified mice lacking ApoE, hematopoietic stem cells did not increase red blood cell production in response to anemia.
Further gene function analysis revealed that when ApoE acts on VLDLR,expensive In hematopoietic stem cells, the activity of the Erg gene, which helps maintain stem cell potential and prevents differentiation into other cells, was attenuated. Interestingly, administration of synthetic ApoE or inhibition of Erg activity made hematopoietic stem cells in healthy mice more likely to produce red blood cells. These results suggest that in response to acute anemia, ApoE is released from VLDL and specifically targets the VLDLR.expensive It promotes hematopoietic stem cells and the body's ability to produce more red blood cells.
The implications of these results could lead to innovative approaches to anemia treatment. Although erythropoietin is already used as a drug to treat anemia, some patients have been shown to have a low response to erythropoietin. Furthermore, current anemia treatments, such as iron supplements and blood transfusions, can lead to iron deposition in the body and cause other health problems. The findings of this study reveal a new mechanism of red blood cell production that differs from previously known pathways and may pave the way for the development of new treatments for patients with severe anemia who have not responded adequately to conventional therapies.
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Sources 2/ https://www.sciencedaily.com/releases/2024/09/240919115053.htm The mention sources can contact us to remove/changing this article |
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