Ion channels in human erythroblasts: Modulation by erythropoietin

Joseph Y. Cheung, Mary Beth Elensky, Ulrike Brauneis, Russell C. Scaduto, Laurie L. Bell, Douglas L. Tillotson, Barbara A. Miller

Research output: Contribution to journalArticle

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Abstract

To investigate the mechanism of intracellular Ca2+ ([Cail) increase in human burst-forming unit-erythroid-derived erythroblasts by erythropoietin, we measured [Cai] with digital video imaging, cellular phosphoinositides with high performance liquid Chromatograph), and plasma membrane potential and currents with whole cell patch clamp. Chelation of extracellular free Ca2+ abolished [Cai] increase induced by erythropoietin. In addition, the levels of inositol-1,4,5-trisphosphate did not increase in erythropoietin-treated erythroblasts. These results indicate that in erythropoietin-stimulated cells, Ca2+ influx rather than intracellular Ca2+ mobilization was responsible for [Cai] rise. Both Ni2+ and moderately high doses of nifedipine blocked [Cai] increase, suggesting involvement of ion channels. Resting membrane potential in human erythroblasts was -10.9±1.0 mV and was not affected by erythropoietin, suggesting erythropoietin modulated a voltage-independent ion channel permeable to Ca2+. No voltage-dependent ion channel but a Ca2+-activated K+ channel was detected in human erythroblasts. The magnitude of erythropoietin-induced [Cai] increase, however, was insufficient to open Ca2+-activated K+ channels. Our data suggest erythropoietin modulated a voltage-independent ion channel permeable to Ca2+, resulting in sustained increases in [Cai].

Original languageEnglish (US)
Pages (from-to)1850-1856
Number of pages7
JournalJournal of Clinical Investigation
Volume90
Issue number5
DOIs
StatePublished - Nov 1992

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Erythroblasts
Erythropoietin
Ion Channels
Calcium-Activated Potassium Channels
Membrane Potentials
Erythroid Precursor Cells
Inositol 1,4,5-Trisphosphate
Nifedipine
Phosphatidylinositols
Cell Membrane

All Science Journal Classification (ASJC) codes

  • Medicine(all)

Cite this

Cheung, J. Y., Elensky, M. B., Brauneis, U., Scaduto, R. C., Bell, L. L., Tillotson, D. L., & Miller, B. A. (1992). Ion channels in human erythroblasts: Modulation by erythropoietin. Journal of Clinical Investigation, 90(5), 1850-1856. https://doi.org/10.1172/JCI116061
Cheung, Joseph Y. ; Elensky, Mary Beth ; Brauneis, Ulrike ; Scaduto, Russell C. ; Bell, Laurie L. ; Tillotson, Douglas L. ; Miller, Barbara A. / Ion channels in human erythroblasts : Modulation by erythropoietin. In: Journal of Clinical Investigation. 1992 ; Vol. 90, No. 5. pp. 1850-1856.
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Cheung, JY, Elensky, MB, Brauneis, U, Scaduto, RC, Bell, LL, Tillotson, DL & Miller, BA 1992, 'Ion channels in human erythroblasts: Modulation by erythropoietin', Journal of Clinical Investigation, vol. 90, no. 5, pp. 1850-1856. https://doi.org/10.1172/JCI116061

Ion channels in human erythroblasts : Modulation by erythropoietin. / Cheung, Joseph Y.; Elensky, Mary Beth; Brauneis, Ulrike; Scaduto, Russell C.; Bell, Laurie L.; Tillotson, Douglas L.; Miller, Barbara A.

In: Journal of Clinical Investigation, Vol. 90, No. 5, 11.1992, p. 1850-1856.

Research output: Contribution to journalArticle

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T1 - Ion channels in human erythroblasts

T2 - Modulation by erythropoietin

AU - Cheung, Joseph Y.

AU - Elensky, Mary Beth

AU - Brauneis, Ulrike

AU - Scaduto, Russell C.

AU - Bell, Laurie L.

AU - Tillotson, Douglas L.

AU - Miller, Barbara A.

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N2 - To investigate the mechanism of intracellular Ca2+ ([Cail) increase in human burst-forming unit-erythroid-derived erythroblasts by erythropoietin, we measured [Cai] with digital video imaging, cellular phosphoinositides with high performance liquid Chromatograph), and plasma membrane potential and currents with whole cell patch clamp. Chelation of extracellular free Ca2+ abolished [Cai] increase induced by erythropoietin. In addition, the levels of inositol-1,4,5-trisphosphate did not increase in erythropoietin-treated erythroblasts. These results indicate that in erythropoietin-stimulated cells, Ca2+ influx rather than intracellular Ca2+ mobilization was responsible for [Cai] rise. Both Ni2+ and moderately high doses of nifedipine blocked [Cai] increase, suggesting involvement of ion channels. Resting membrane potential in human erythroblasts was -10.9±1.0 mV and was not affected by erythropoietin, suggesting erythropoietin modulated a voltage-independent ion channel permeable to Ca2+. No voltage-dependent ion channel but a Ca2+-activated K+ channel was detected in human erythroblasts. The magnitude of erythropoietin-induced [Cai] increase, however, was insufficient to open Ca2+-activated K+ channels. Our data suggest erythropoietin modulated a voltage-independent ion channel permeable to Ca2+, resulting in sustained increases in [Cai].

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Cheung JY, Elensky MB, Brauneis U, Scaduto RC, Bell LL, Tillotson DL et al. Ion channels in human erythroblasts: Modulation by erythropoietin. Journal of Clinical Investigation. 1992 Nov;90(5):1850-1856. https://doi.org/10.1172/JCI116061