Effects of Dexamethasone on Bone Marrow Erythropoiesis

Malgor, L.A.; Torales, Pedro R.; Klainer, E; Barrios, Luis; Blanc, C

doi:10.1159/000178640

Cited by 18 publications

(13 citation statements)

References 5 publications

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“…74 showed an antagonistic effect on the T3 action. This blocking effect of T 4 on T 3 action is unusual, since the biological potence of T4 is similar or lower than T3, but both hormones act in the same direction [19][20][21][27][28][29]. This finding represents, to the best of our knowledge, the first observation of an hormonal blocking action of the T4 on T 3.…”

Section: Blocking Effect Of T4 On the Ts Actionsupporting

confidence: 50%

See 1 more Smart Citation

Thyroid hormone actions and membrane fluidity Blocking action thyroxine on triiodothyronine effect

Mendoza¹,

Moreno²,

Massa³

et al. 1977

FEBS Letters

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Section: Blocking Effect Of T4 On the Ts Actionsupporting

confidence: 50%

“…However, several workers suggested that T4 could have a true biological activity per se [27][28][29]. Some membrane systems were affected by thyroid hormones [30][31][32][33] ; in our case, T3 decreased membrane fluidity.…”

Section: Blocking Effect Of T4 On the Ts Actionmentioning

confidence: 43%

Thyroid hormone actions and membrane fluidity Blocking action thyroxine on triiodothyronine effect

Mendoza¹,

Moreno²,

Massa³

et al. 1977

FEBS Letters

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“…Addison's disease in man is associated with normocytic, normochromic anemia (18), and a congenital erythroid hy- poplasia of children (Diamond-Blackfan syndrome) is frequently responsive to low doses of glucocorticoids (19). In animals, glucocorticosteroids and ACTH have been reported to stimulate erythropoiesis (20)(21)(22) but inhibition has also been observed (23,24) On the basis. of observations in nephrectomized rats, Malgor and coworkers (22) concluded that dexamethasone stimulated erythropoiesis by an effect on erythropoietin production.…”

Section: Introductionmentioning

confidence: 99%

“…In animals, glucocorticosteroids and ACTH have been reported to stimulate erythropoiesis (20)(21)(22) but inhibition has also been observed (23,24) On the basis. of observations in nephrectomized rats, Malgor and coworkers (22) concluded that dexamethasone stimulated erythropoiesis by an effect on erythropoietin production. Glucocorticoids are also reported to stimulate erythropoiesis in amphibians (25).…”

Section: Introductionmentioning

confidence: 99%

Potentiation of erythropoiesis in vitro by dexamethasone.

Golde¹,

Bersch²,

Cline³

1976

J. Clin. Invest.

141

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A B S T R A C T The effect of dexamethasone on erythropoiesis was examined in vitro. Hematopoietic cells from 13-day mouse fetal livers were cultured for 48 h in the presence or absence of erythropoietin and erythroid colonies enumerated. Colony formation occurring in cultures containing no added erythropoietin was inhibited by the incorporation of antierythropoietin antibody, suggesting that these colonies formed in response to endogenous hepatic erythropoietin. Maximal colony formation was observed with 0.5 U/ml of sheep erythropoietin. Dexamethasone increased erythroid colony formation with peak stimulation at 10-M. Dexamethasone potentiation was most marked in cultures containing less than maximally stimulating concentrations of erythropoietin. The cells required only a brief exposure to glucocorticosteroid to exhibit the augmented cloning capacity, and dexamethasone stimulation was inhibited by progesterone (10 M). A comparable response to dexamethasone was observed in cultures of adult murine and human bone marrow erythroid progenitors, implying that the phenomenon is not peculiar to fetal cells and is not dependent on the presence of fetal hepatocytes. These data suggest that erythroid progenitor cells possess a glucocorticoid receptor mechanism that can modulate the response to erythropoietin in vitro.

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“…It is noteworthy that the TR␣ isoform is expressed preferentially in differentiating erythroid cells (14) and that the v-erbA oncogene involved in avian erythroleukemia represents a mutated form of TR␣ (15,16). Studies with whole animals have indicated that T 3 stimulates erythropoiesis (17), whereas in vitro assays have shown that T 3 inhibits colony formation by erythroid progenitors (18,19). The elegant studies of Beug and colleagues (19 -24) have demonstrated that the balance between proliferation and differentiation can be altered by the introduction of exogenous TR␣ (cerbA) or v-erbA into immature avian red blood cells.…”

mentioning

confidence: 99%

Thyroid Hormone Receptor-interacting Protein 1 Modulates Cytokine and Nuclear Hormone Signaling in Erythroid Cells

Ingley¹,

Chappell²,

Poon³

et al. 2001

Journal of Biological Chemistry

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Erythropoietin (Epo) and thyroid hormone (T 3 ) are key molecules in the development of red blood cells. We have shown previously that the tyrosine kinase Lyn is involved in differentiation signals emanating from an activated erythropoietin receptor. Here we demonstrate that Lyn interacts with thyroid hormone receptor-interacting protein 1 (Trip-1), a transcriptional regulator associated with the T 3 receptor, providing a link between the Epo and T 3 signaling pathways. Trip-1 co-localized with Lyn and the T 3 receptor ␣ in the cytoplasm/plasma membrane of erythroid cells but translocated to discrete nuclear foci shortly after Epo-induced differentiation. Our data reveal that T 3 stimulated the proliferation of immature erythroid cells, and inhibited maturation promoted by erythropoietin. Removal of T 3 reduced cell division and enhanced terminal differentiation. This was accompanied by large increases in the cell cycle inhibitor p27Kip1 and by increasing expression of erythroid transcription factors GATA-1, EKLF, and NF-E2. Strikingly, a truncated Trip-1 inhibited both erythropoietin-induced maturation and T 3 -initiated cell division. This mutant Trip-1 acted in a dominant negative fashion by eliminating endogenous Lyn, elevating p27 Kip1 , and blocking T 3 response elements. These data demonstrate that Trip-1 can simultaneously modulate responses involving both cytokine and nuclear receptors.

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Effects of Dexamethasone on Bone Marrow Erythropoiesis

Cited by 18 publications

References 5 publications

Thyroid hormone actions and membrane fluidity Blocking action thyroxine on triiodothyronine effect

Thyroid hormone actions and membrane fluidity Blocking action thyroxine on triiodothyronine effect

Potentiation of erythropoiesis in vitro by dexamethasone.

Thyroid Hormone Receptor-interacting Protein 1 Modulates Cytokine and Nuclear Hormone Signaling in Erythroid Cells

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