Erythropoietin mRNA levels are governed by both the rate of gene transcription and posttranscriptional events

Gertz, MA; Gaut, CC; Bunn, H. Franklin

doi:10.1182/blood.v77.2.271.271

Cited by 190 publications

(17 citation statements)

References 25 publications

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“…The serum of c-mpl -/mice, like that of other thrombocytopenic animals, contains high levels of TPO [13,[33][34][35]. To explain the inverse relationship between platelet count and circulating TPO level, it was tempting to speculate that a sensing mechanism was responsible for detecting lower platelet counts and stimulating TPO transcription in a similar way that EPO transcription is regulated in response to anemia and low oxygen pressure [36][37][38].…”

Section: Regulation Of Tpo Productionmentioning

confidence: 99%

Hematopoietic Deficiencies in c‐mpl and TPO Knockout Mice

1998

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Section: Regulation Of Tpo Productionmentioning

confidence: 99%

Hematopoietic Deficiencies in c‐mpl and TPO Knockout Mice

1998

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“…Hypoxic induction of the Epo gene appears to be regulated by both transcriptional and post-transcriptional mechanisms. (12)(13)(14) Hypoxia-inducible factor 1 (HIF-1) was identified as a protein that specifically binds to an enhancer element 3′ to the Epo gene in a hypoxia-regulated fashion. (15,16) HIF-1 is a key regulator of responses to hypoxia, occupying a central position in oxygen homeostasis in a wide range of organisms.…”

mentioning

confidence: 99%

Antitumor effects of 2‐oxoglutarate through inhibition of angiogenesis in a murine tumor model

et al. 2009

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“…This systemic adaptation is triggered by oxia. Moreover, aldolase A [12, 13], glycero-3-phosphate dehyinduction of erythropoietin, a hematopoietic hormone, whose drogenase [14], phosphoglycerate kinase [15], non-neural enogene is transcriptionally up-regulated in endothelial cells in the lase [16] and lactate dehydrogenase A [13,17], non-rate-limiting kidney by reduced O2 tension [4,5]. enzymes, are also up-regulated by hypoxia.…”

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confidence: 99%

Hypoxia‐induced expression of phosphoglycerate mutase B in fibroblasts

Takahashi

Yoshimi

et al. 1998

European Journal of Biochemistry

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Molecular oxygen (O 2 ) is essential for aerobic organisms. Exposure of tissues or cells to hypoxia induces a variety of adaptive or pathogenic responses. To understand the mechanism and processes of cellular response to hypoxia, we exposed fetal rat lung fibroblasts to hypoxia (pO 2 Ϸ5 Pa) and screened the hypoxia-responsible gene by the differential display method. Exposure of the cells to hypoxia activated the phosphoglycerate mutase B (PGM-B) gene, resulting in the induction of PGM enzymatic activity, concomitant with elevations of PGM-B mRNA and protein levels. The mRNA level was elevated linearly with decreases in partial O 2 pressure, indicating a 2Ϫ3-fold increase in these levels after 16 h hypoxia. Up-regulation of PGM mRNA by hypoxia was obvious after 8 h exposure, reached its peak after 16 h, persisting for 40 h and returned to the basal level after reoxygenation at 20% O 2 for 16 h. Run-on and stability assays indicated that PGM-B expression is regulated mainly at the transcriptional step. These results suggest that the induction of PGM-B may contribute to the regulation of the glycolytic flux under reduced O 2 tension and play a role in the adaptation of cells to hypoxia.Keywords : hypoxia ; reoxygenation ; phosphoglycerate mutase B; differential display; fibroblast.Molecular oxygen (O 2 ) is essential for aerobic organisms. within minutes, after hypoxic exposure. It is generally accepted Principally, O 2 participates in oxidation-reduction reactions in that the Pasteur effect relates to an acute increase in the intracelthe biosystem and functions as a terminal electron acceptor of lular phosphofructokinase activity resulting from changes in the mitochondrial oxidative phosphorylation in the production of en-concentration of low molecular-mass allosteric effectors, alergy [1]. O 2 is also the means of oxygenation by which bioactive though other alterations in enzyme activities participate [6,7]. materials, such as steroid hormones and prostaglandins, are syn-Chronic hypoxic exposure of a variety of tissues and cells results thesized. Furthermore, desaturation of fatty acid and hydroxyla-in a substantial additional increase in the rate of glycolysis betion of proline also require O 2 for enzymatic reactions. The par-yond that produced by the Pasteur effect [8]. tial O 2 pressure needed for enzymatic reactions varies depending Enzymatic activities of all glycolytic components of epitheon the type of enzyme [2].lial and mesenchymal cell lines are coordinately enhanced by Ischemia and/or hypoxia cause a reduced tension of O 2 in chronic hypoxia [9,10]. Although the detailed mechanism by cells and tissues. In an acute response to reduced O 2 concentra-which the glycolytic activity is substantially increased after tions in tissues, hyperventilation is the primary systemic adapta-chronic hypoxia is unclear, some glycolytic enzymes, but not tion. It results in an increase in arterial O2 tension, enhancing all, are up-regulated at transcription levels. Steady-state mRNA delivery of O 2 to distal tissues [3]....

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Erythropoietin mRNA levels are governed by both the rate of gene transcription and posttranscriptional events

Cited by 190 publications

References 25 publications

Hematopoietic Deficiencies in c‐mpl and TPO Knockout Mice

Hematopoietic Deficiencies in c‐mpl and TPO Knockout Mice

Antitumor effects of 2‐oxoglutarate through inhibition of angiogenesis in a murine tumor model

Hypoxia‐induced expression of phosphoglycerate mutase B in fibroblasts

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