Disease relevance of Erythropoiesis

• We conclude that in patients who have undergone renal transplantation, slight increases in endogenous erythropoietin levels induce erythropoiesis to the same extent as do large doses of exogenous erythropoietin in patients with uremia [1].
• Effects of oxygen inhalation on endogenous erythropoietin kinetics, erythropoiesis, and properties of blood cells in sickle-cell anemia [2].
• Heterozygous deficiency of hypoxia-inducible factor-1alpha (HIF-1alpha), which mediates the cellular response to hypoxia by increasing expression of genes involved in erythropoiesis and angiogenesis, has been previously shown to delay hypoxia-induced pulmonary hypertension [3].
• Identification of spermine as an inhibitor of erythropoiesis in patients with chronic renal failure [4].
• These data suggest that angiotensin II facilitates erythropoiesis, a conclusion with implications for the management of chronically ill patients on inhibitors of the renin-angiotensin system [5].

Psychiatry related information on Erythropoiesis

• At the same time, haloperidol and, especially, cyproheptadine normalized suppressed erythropoiesis and modulated activated granulocytopoiesis under conditions of paradoxical sleep deprivation [6].

High impact information on Erythropoiesis

• The p38alpha MAP kinase plays a critical role linking developmental and stress-induced erythropoiesis through regulation of Epo expression [7].
• To test the hypothesis that the Trf cycle has unique importance for erythropoiesis, we disrupted the Trfr gene in mice [8].
• Mice lacking Trfr have a more severe phenotype than hpx mice, affecting both erythropoiesis and neurologic development [8].
• Stat5 is rapidly activated following EpoR stimulation, but its function in erythropoiesis has been unclear since adult Stat5a-/-5b-/- mice have normal steady-state hematocrit [9].
• SOCS3 is essential in the regulation of fetal liver erythropoiesis [10].

Chemical compound and disease context of Erythropoiesis

• Friend murine erythroleukemia cells underwent apparently normal erythropoiesis when treated with dimethyl sulfoxide [11].
• Aplastic anemia with fetallike erythropoiesis following androgen therapy [12].
• Pure red cell aplasia (PRCA): Response of three patients of cyclophosphamide and/or antilymphocyte globulin (ALG) and demonstration of two types of serum IgG inhibitors to erythropoiesis [13].
• Response of Diamond-Blackfan anemia to metoclopramide: evidence for a role for prolactin in erythropoiesis [14].
• These and additional data stemming from inhibition of heme synthesis with succinylacetone or from iron overload suggest that highly efficient utilization of iron in mitochondrial heme synthesis during normal erythropoiesis alters the regulation of iron metabolism via the IRE/IRP system [15].

Biological context of Erythropoiesis

• DNA ligase I is required for fetal liver erythropoiesis but is not essential for mammalian cell viability [16].
• The data provided demonstrate that Jak2 has pivotal functions for signal transduction of a set of cytokine receptors required in definitive erythropoiesis [17].
• EPOR-F may transduce a signal to prevent programmed cell death that is independent of the mitogenic signal, and alternative splicing of the EPOR gene may have an important role in erythropoiesis [18].
• Hypoxia-inducible factor 1 (HIF-1) is a master regulator of oxygen homeostasis that controls angiogenesis, erythropoiesis, and glycolysis via transcriptional activation of target genes under hypoxic conditions [19].
• Here, we analyze the impact of the GR on erythropoiesis in vivo, using GR-deficient mice or mice expressing a GR defective for transactivation [20].

Anatomical context of Erythropoiesis

• To clarify the abnormalities in erythropoiesis, we studied erythropoietin production in the older sibling as well as in vivo and in vitro responses of bone marrow to various stimuli [21].
• Mutations in the KIT transmembrane protein-tyrosine kinase receptor affect erythropoiesis, resulting in fewer committed late progenitors (colony-forming unit erythroid, CFU-E) in the fetal liver [22].
• The cells resemble proerythroblasts and, when exposed to dimethyl sulphoxide (DMSO) or a variety of other chemicals, can be induced to undergo a programme of differentiation which closely resembles the final stages of normal erythropoiesis [23].
• Erythropoietin-independent erythrocyte production: signals through gp130 and c-kit dramatically promote erythropoiesis from human CD34+ cells [24].
• Moreover, while the effects on erythropoiesis in normal animals were modest, TPO greatly expanded the number of erythroid progenitors and blood reticulocytes and was associated with accelerated red cell recovery in myelosuppressed mice [25].

Associations of Erythropoiesis with chemical compounds

• These data provide an explanation for the preferential suppression of erythropoiesis observed clinically in ethanol abuse [26].
• We have found that the Epo gene is a direct transcriptional target gene of retinoic acid signaling during early erythropoiesis (prior to embryonic day E12.5) in the fetal liver [27].
• His major findings during this period were the discovery that hydrocortisone and corticosterone stimulated erythropoiesis (1958) and that cobalt increased erythropoietin production in the isolated perfused dog kidney (1961) [28].
• Effect of perturbation of specific folate receptors during in vitro erythropoiesis [29].
• Lack of angiotensin II-facilitated erythropoiesis causes anemia in angiotensin-converting enzyme-deficient mice [5].

Gene context of Erythropoiesis

• Both types of mutations exhibited identical phenotypes, indicating that EPO and the EPOR are crucial for definitive erythropoiesis in vivo and that no other ligands or receptors can replace them [30].
• Homozygous inactivation of the Rb gene in the mouse leads to mid-gestational lethality with defects in erythropoiesis and neurogenesis [31].
• Slc11a2 is required for intestinal iron absorption and erythropoiesis but dispensable in placenta and liver [32].
• In addition, the proliferative reserves of hematopoietic progenitors and stress erythropoiesis were significantly reduced in Ercc1-/- mice compared to age-matched controls [33].
• Since both RBTN2 and TAL1 are crucial for normal erythropoiesis, these data have important implications for transcription networks therein [34].

Analytical, diagnostic and therapeutic context of Erythropoiesis

• S1 nuclease and primary transcript in situ hybridization analyses demonstrate that all seven murine globin genes (zeta, alpha1, alpha2, epsilony, betaH1, betamaj, and betamin) are transcribed during primitive erythropoiesis, however transcription of the zeta, epsilony, and betaH1 genes is restricted to the primitive erythroid lineage [35].
• Hematopoietic stem cells in Friend murine leukemia virus-infected mice undergoing chemotherapy: remission and relapse of erythropoietin-independent erythropoiesis induced by hydroxyurea [36].
• Erythropoietin (EPO), well known for its role in stimulation of erythropoiesis, has recently been shown to have a dramatic neuroprotective effect in animal models of cerebral ischemia, mechanical trauma of the nervous system, and excitotoxins, mainly by reducing apoptosis [37].
• Northern blot analysis indicated that p55 mRNA was constitutively expressed during erythropoiesis and underwent 2-fold amplification after induction of K562 erythroleukemia cells toward the erythropoietic lineage [38].
• Since patients with SCD frequently develop mixed hematopoietic chimerism after allogeneic nonmyeloablative stem cell transplantation, we used this opportunity to directly compare the differentiation and survival of SCD and donor-derived erythropoiesis in vivo [39].

References