Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P20020 (adenosine triphosphatase)
 3,299 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Treatment of Friend erythroleukemia cells with several different chemical agents causes an early decrease in the 86Rb+ influx mediated by Na+/K+ adenosine triphosphatase (ATPase). These agents, which induce Friend cells to differentiate, include dimethylsulfoxide (DMSO), ouabain, hypoxanthine, and actinomycin D. The magnitude of the early decrease in 86Rb+ influx correlates with the proportion of cells in cultures of inducible Friend cell clones which later go on to synthesize hemoglobin. Compounds which do not incude differentiation in these cells, such as xanthine, exogenous hematin, and erythropoietin, do not cause a change in 86Rb+ influx. A change in the intracellular K+ ion concentration does not occur during induction by DMSO because, although there is a decrease in K+ content per cell soon after induction, there is a parallel decrease in cell volume. These results and previous observations from this laboratory are discussed in terms of the posible involvement of the Na+/K+ ATPase in Friend cell differentiation.
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PMID:The program of Friend cell erythroid differentiation: early changes in Na+/K+ ATPase function. 21 40

Recombinant human erythropoietin (epoetin) is widely used for the treatment of renal anemia. The aim of our study was to determine the influence of epoetin on erythrocyte metabolism. Thirty-six hemodialysis patients (22 men, 14 female), aged from 17 to 64 years (mean age 43) and 30 healthy volunteers (12 men, 18 female), aged from 25 to 65 years (mean age 40) were studied. Epoetin (Eprex, Janssen-Cilag) was administered subcutaneously with the starting dose of 2000 IU three times per week for twelve months (range from 75 to 133 IU/kg/week, mean dose 102+/-21 IU/kg/week). Laboratory markers of: hematological response, iron status and erythrocyte metabolism were measured before epoetin administration. Afterwards the markers were controlled every three months. During epoetin treatment a significant increase in hemoglobin concentration was observed (100% patients responded in a positive way to epoetin). The following changes in erythrocyte metabolism were noticed: 1) in glycolytic enzymes: a significant increase in the activity of hexokinase and that of lactate dehydrogenase, 2) in glycolytic intermediates: a significant increase in the 2,3-diphosphoglycerate and adenosine triphosphate concentrations, 3) a significant increase sodium, potassium adenosine triphosphatase concentration, 4) the glucose uptake by erythrocytes significantly decreased while the lactate production remained stable. During anemia treatment with epoetin in hemodialysis patients not only quantitative but also qualitative changes in erythrocytes were observed.
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PMID:Erythrocyte metabolism during renal anemia treatment with recombinant human erythropoietin. 1563 50

Because kidneys consume a large amount of oxygen and are relatively inefficient in oxygen uptake, they are susceptible to hypoxia, especially in patients with advanced chronic kidney disease accompanied by loss of peritubular capillaries. Accumulating evidence suggests that chronic tubulointerstitial hypoxia acts as a final common pathway leading to end-stage renal disease. Some biologically active uremic retention molecules, considered as uremic toxins, accumulate as the renal function declines, and at this moment, more than 90 bioactive uremic toxins have been identified. Uremic toxins per se have been proven to accelerate the progression of renal failure. However, the causal relationship between uremic toxin and tubulointerstitial hypoxia remains unclear. Our studies provided direct evidence that uremic toxin dysregulates oxygen metabolism in the kidney. Indoxyl sulfate (IS), a representative protein-bound uremic toxin, increased oxygen consumption in proximal renal tubules, decreased renal oxygenation, and consequently aggravated hypoxia in the remnant rat kidneys. The increase in tubular oxygen consumption by IS was dependent on sodium-potassium adenosine triphosphatase and oxidative stress. Our work also indicated a possible connection between IS and the desensitization of the oxygen-sensing mechanism in erythropoietin-producing cells, which may partly explain inadequate erythropoietin production in hypoxic kidneys of end-stage renal disease patients. Studies of uremic toxins will open a new avenue in development of novel therapeutic approaches of kidney disease.
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PMID:Dysregulated oxygen metabolism of the kidney by uremic toxins: review. 2220 Apr 19