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

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35 Scopus citations


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
Issue number5
StatePublished - Nov 1992

All Science Journal Classification (ASJC) codes

  • General Medicine


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