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Usage Information

Effect of perturbation of specific folate receptors during in vitro erythropoiesis.
A C Antony, E Bruno, R A Briddell, J E Brandt, R S Verma, R Hoffman
A C Antony, E Bruno, R A Briddell, J E Brandt, R S Verma, R Hoffman
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Research Article

Effect of perturbation of specific folate receptors during in vitro erythropoiesis.

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Abstract

Although antisera to specific placental folate receptors inhibits the uptake of 5-methyltetrahydrofolate into cultured malignant human cells, little is known of the functional significance of folate receptors in normal human cells. Human bone marrow cells were therefore assayed for erythropoietic burst-forming units in the presence of an antihuman placental folate receptor serum and preimmune serum to determine the role of such a receptor in erythroid differentiation. When marrow cells were assayed in the presence of anti-receptor antiserum, there was (i) a threefold increase in erythropoietic burst formation and a twofold increase in the number of cells per erythroid burst; (ii) morphological evidence for nuclear/cytoplasmic dissociation of orthochromatic normoblasts composing erythroid bursts (megaloblastic erythropoiesis); (iii) intracellular folate deficiency with a 70% reduction of intracellular folate in antiserum treated cells as compared with control cells; and (iv) complete reversal of antiserum-induced changes on preincubation of antiserum with purified human placental folate receptor. These data support the conclusion that folate receptors on marrow cells provide an important function in the cellular uptake of folates during in vitro erythropoiesis. This process of folate uptake also appears to play a pivotal role in the differentiation and proliferation of erythroid progenitor cells.

Authors

A C Antony, E Bruno, R A Briddell, J E Brandt, R S Verma, R Hoffman

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Usage data is cumulative from November 2025 through November 2026.

Usage JCI PMC
Text version 376 18
PDF 197 10
Scanned page 602 1
Citation downloads 258 0
Totals 1,433 29
Total Views 1,462
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ISSN: 0021-9738 (print), 1558-8238 (online)

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