Inhibition of dimethyl sulfoxide-stimulated Friend cell erythrodifferentiation by hydrocortisone and other steroids.

doi:10.1073/PNAS.75.8.3851

Paper

Inhibition of dimethyl sulfoxide-stimulated Friend cell erythrodifferentiation by hydrocortisone and other steroids.

Published Aug 1, 1978 · W. Scher, D. Tsuei, S. Sassa

Proceedings of the National Academy of Sciences of the United States of America

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64

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Abstract

Erythrodifferentiation and hemoglobin synthesis in dimethyl sulfoxide-stimulated Friend erythroleukemia cells were inhibited by hydrocortisone (HC) and four other steroids: dexamethasone, deoxycorticosterone, corticosterone, and aldosterone. The effect was specific, because no significant cytotoxicity occurred with any of these compounds at the concentrations that were inhibitory. The mechanism of action of HC was studied in detail. In the absence of dimethyl sulfoxide, it had no effect on hemoglobin levels; but, in the presence of this inducer, the synthesis of heme and globin were each inhibited by approximately 90%. There was no alteration in the synthesis of any major protein other than globin, as determined by gel electrophoresis of cell lysates. The activities of two enzymes in the heme biosynthetic pathway, delta-aminolevulinate dehydratase and uroporphyrinogen-I synthase, were inhibited by 80% and 70%, respectively. Globin mRNA induction was reduced by approximately 90%. This demonstrated that the HC inhibition of globin synthesis occurred at a pretranslational step. The dimethyl sulfoxide-induced single-stranded breaks in DNA, which have been suggested to play a role in Friend leukemia cell differentiation, were reduced in number but not eliminated. HC reduced the dimethyl sulfoxide-stimulation of virus release into the medium by approximately 50%. HC treatment in the absence of dimethyl sulfoxide doubled the production of virus.

In Vitro Study

Study Snapshot

Hydrocortisone and other steroids effectively inhibit dimethyl sulfoxide-stimulated Friend erythroleukemia cell erythrodifferentiation and hemoglobin synthesis, with no significant cytotoxicity observed.

PopulationOlder adults (50-71 years)

Sample size24

MethodsObservational

OutcomesBody Mass Index projections

ResultsSocial networks mitigate obesity in older groups.

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Paper

Inhibition of dimethyl sulfoxide-stimulated Friend cell erythrodifferentiation by hydrocortisone and other steroids.

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References

Citations

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Mmip-2/Rnf-17 enhances c-Myc function and regulates some target genes in common with glucocorticoid hormones, providing a molecular basis for their common cellular functions.

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Estrogens suppress erythropoiesis by repressing the erythroid transcription factor GATA-1 through protein-protein interaction with the estrogen receptor, potentially affecting cellular differentiation.

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Vitamin D3 can induce differentiation in murine erythroleukemia cells, with an optimum concentration of 750 nM, similar to DMSO, and inhibited by dexamethasone.

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Decreases in ALA dehydratase activity by chemical intoxication and genetic disorders can suppress heme biosynthesis, highlighting the importance of this enzyme in heme biosynthesis.

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The glucocorticoid receptor inhibits erythroleukemia cell differentiation by interfering with GATA-1 function, potentially explaining its inhibitory effect on erythroid differentiation in MEL cells.

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Differentiation-induced reduction in lactate accumulation in leukemia cells correlates with the initiation of terminal cell division, making them useful models for studying lactate formation in malignant cells.

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The blocked functions in the erythroleukemia cell differentiation pathway may serve as a major control mechanism for commitment, with cytochalasin B-based assays providing a direct monitoring method.

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TPA regulates c-fms gene expression through a dexamethasone-sensitive mechanism, and c-fms mRNA levels are controlled by arachidonic acid metabolites.