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In this study we observed a threshold for effective transplantation of HO-1 knockout bone marrow too few cells led to hematopoietic failure due to stem cell depletion, transplantation using cell numbers above this threshold were successful, but serial transplants from these recipient animals also resulted in hematopoietic failure.
However, hmox +/− HSCs were ineffective in the radioprotection and serial repopulation of myeloablated recipients. Mice lacking one allele of HO-1 ( hmox +/−) showed accelerated hematopoietic recovery from myelotoxic injury.
We previously reported that HO-1 deficiency leads to disrupted stress hematopoiesis of stem cells and progenitors. In a rare human case, HO-1 deficiency was associated with thrombocytosis, coagulation abnormalities, persistent hemolytic anemia, iron deposition in tissues, and premature death. Genetic knockout (KO) of HO-1 results in partial embryonic lethality and leads to a number of hematological disorders in surviving mice, including anemia, hypoferremia and tissue accumulation of iron. HO activity has been implicated in the control of inflammation, immune regulation and organ transplantation. HO-1 facilitates iron reutilization in mammals and modulates the expression of cytokines and adhesion molecules. CO is a diffusible regulator that has been linked to the regulation of numerous cellular and tissue functions.
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The free iron from this reaction is sequestered by ferritin, and the biliverdin is rapidly converted into bilirubin by biliverdin reductase. The heme oxygenase-1 enzyme (HO-1) is encoded by the hmox-1 gene and is an inducible stress enzyme that catalyzes heme oxidation into carbon monoxide (CO), free ferrous iron, and biliverdin. Factors that distinguish homeostatic and stress hematopoiesis are less well described. These include erythropoietin, iron, cytokines, cellular regulators, and adhesion molecules.
This process occurs in part within the spleen and is regulated by several factors that are shared with homeostatic erythropoiesis. In response to special needs, such as after bone marrow (BM) transplantation, myelosuppression, or anemia, stress erythropoiesis occurs as the body attempts to increase the production of erythrocytes. Homeostatic erythropoiesis maintains normal hematocrit levels and occurs as needed to replace old and damaged erythrocytes. As reticulocytes, they exit the bone marrow and enter blood capillaries to participate in oxygen transport. Just prior to maturation, erythroblasts extrude their nucleus and mature into reticulocytes. Erythropoiesis, the development of mature red blood cells (RBCs), originates from pluripotent hematopoietic stem cells (HSCs) and progresses through erythroblasts to the formation of RBCs.
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