Erythropoiesis in vitro. Role of calcium.

Misiti, J; Spivak, Jerry L.

doi:10.1172/jci109618

Cited by 70 publications

(32 citation statements)

References 27 publications

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“…Our current study clearly demonstrates that a transient rise in [Cak] occurs rapidly in early erythroid precursors exposed to erythropoietin or GM-CSF. Taken together, our data, as well as previous observations (20)(21)(22)(23)(24) (Fig. 1, B (Fig.…”

Section: Discussionsupporting

confidence: 92%

“…Studies in normal and leukemia cell lines have implicated a role for intracellular Ca2" in the mechanism of action of erythropoietin. Erythropoietin-induced murine erythroid colony growth was enhanced by the ionophore A23 187 but inhibited by treatment with EGTA, a nonspecific chelator of Ca2" (20). Other indirect evidence implicating [Cak] and Kay have also demonstrated an increase in intracellular free calcium in a select population of normal bone marrow mononuclear cells and membrane depolarization of benzidine-positive nucleated marrow cells in response to erythropoietin (23,24).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Erythropoietin stimulates a rise in intracellular free calcium concentration in single early human erythroid precursors.

Miller¹,

Scaduto²,

Tillotson³

et al. 1988

J. Clin. Invest.

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Erythropoietin and granulocyte-macrophage colony-stimulating factor (GM-CSF) stimulate the differentiation and proliferation of erythroid cells. To determine the cellular mechanism of action of these growth factors, we measured changes in intracellular free calcium concentration (jCaJ) in single human erythroid precursors in response to recombinant erythropoietin and GM-CSF. [CaJ in immature erythroblasts derived from cultured human cord blood erythroid progenitors was measured with fluorescence microscopy digital video imaging.When stimulated with erythropoietin, [CaJ in the majority of erythroblasts increased within 3 min, peaked at 5 min, and returned toward baseline at 10 min. The percentage of cells that responded to erythropoietin stimulation increased in a dose-dependent manner. Additional stimulation with GM-CSF in cells previously exposed to erythropoietin resulted in a second [Ca¢J increase. Immature erythroblasts treated with GM-CSF followed by erythropoietin responded similarly to each factor with a rise in [Ck]. The source of transient calcium is intracellular since erythroblasts were incubated in medium devoid of extracellular calcium. Our observations suggest that changes in [CaJ may be an intracellular signal that mediates the proliferative/differentiating effect of hematopoietic growth factors.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Erythropoietin stimulates a rise in intracellular free calcium concentration in single early human erythroid precursors.

Miller¹,

Scaduto²,

Tillotson³

et al. 1988

J. Clin. Invest.

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“…GallienLartigue (53) found that a calcium ionophore (A-23187) stimulated the proliferation rate of the hematopoietic stem cells of the mouse bone marrow as assayed by spleen colony-forming method (53). Finally, Misiti and Spivak (54) reported that small concentrations of calcium ionophore A-23187 (10 nM) enhanced Ep-induced erythroid colony formation.…”

Section: Discussionmentioning

confidence: 99%

Effect of parathyroid hormone on erythropoiesis.

Meytes¹,

Bogin²,

Ma³

et al. 1981

J. Clin. Invest.

224

112

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A B S T R A C T Inhibitors of erythropoiesis have been found in the blood of uremic patients but their nature has not been identified. These patients have excess blood levels of parathyroid hormone (PTH) and it is possible that PTH inhibits erythropoiesis. The present study was undertaken to examine the effect of intact PTH molecules and some of its fragments on human peripheral blood and mouse bone marrow burst-forming units-erythroid (BFU-E), on mouse bone marrow erythroid colony-forming unit (CFU-E), and granulocyte macrophage progenitors (CFU-GM), and evaluate the interaction between PTH and erythropoietin (Ep) on human BFU-E. Intact PTH (1-84 bPTH) in concentrations (7.5-30 U/ml) comparable to those found in blood of uremic patients produced marked and significant (P < 0.01) inhibition of BFU-E and mouse marrow GFU-GM, but not of mouse marrow CFU-E. Inactivation of 1-84 bPTH abolished its action on erythropoiesis. Increasing the concentration of Ep in the media from 0.67 to 1.9 U/ml overcame the inhibitory effect of 1-84 bPTH on BFU-E. The N-terminal fragment of PTH (1-34 bPTH) and 53-84 hPTH had no effect on BFU-E.The results deomonstrate that (a) either the intact PTH molecule or a C-terminal fragment(s) bigger than 53-84 moiety exerts the inhibitory effect on erythropoiesis, and (b) adequate amounts of Ep can overcome this action of PTH. The data provide one possible pathway for the participation of excess PTH in the genesis of the anemia of uremia.

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“…Lines Using RT-PCR-The ability of erythropoietin to stimulate calcium influx in murine erythroid cells and erythroleukemia cell lines has been demonstrated previously (7)(8)(9)(10)(11)23). Here, to explore whether this influx occurred through the classical TRP channels, the expression of TRPC1 to -6 was examined in HCD-57 murine erythroleukemia cells and in Ba/F3 Epo-R cells, a hematopoietic cell line stably transfected with murine Epo-R and previously shown to respond to Epo with a rise in [Ca] i (23).…”

Section: Expression Of Trpc In Murine Tissues and Erythroid Cellmentioning

confidence: 98%