Go to JCI Insight
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Publication alerts by email
  • Advertising
  • Job board
  • Contact
  • Clinical Research and Public Health
  • Current issue
  • Past issues
  • By specialty
    • COVID-19
    • Cardiology
    • Gastroenterology
    • Immunology
    • Metabolism
    • Nephrology
    • Neuroscience
    • Oncology
    • Pulmonology
    • Vascular biology
    • All ...
  • Videos
    • Conversations with Giants in Medicine
    • Video Abstracts
  • Reviews
    • View all reviews ...
    • Complement Biology and Therapeutics (May 2025)
    • Evolving insights into MASLD and MASH pathogenesis and treatment (Apr 2025)
    • Microbiome in Health and Disease (Feb 2025)
    • Substance Use Disorders (Oct 2024)
    • Clonal Hematopoiesis (Oct 2024)
    • Sex Differences in Medicine (Sep 2024)
    • Vascular Malformations (Apr 2024)
    • View all review series ...
  • Viewpoint
  • Collections
    • In-Press Preview
    • Clinical Research and Public Health
    • Research Letters
    • Letters to the Editor
    • Editorials
    • Commentaries
    • Editor's notes
    • Reviews
    • Viewpoints
    • 100th anniversary
    • Top read articles

  • Current issue
  • Past issues
  • Specialties
  • Reviews
  • Review series
  • Conversations with Giants in Medicine
  • Video Abstracts
  • In-Press Preview
  • Clinical Research and Public Health
  • Research Letters
  • Letters to the Editor
  • Editorials
  • Commentaries
  • Editor's notes
  • Reviews
  • Viewpoints
  • 100th anniversary
  • Top read articles
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Publication alerts by email
  • Advertising
  • Job board
  • Contact
Top
  • View PDF
  • Download citation information
  • Send a comment
  • Terms of use
  • Standard abbreviations
  • Need help? Email the journal
  • Top
  • Abstract
  • Version history
  • Article usage
  • Citations to this article

Advertisement

Research Article Free access | 10.1172/JCI116061

Ion channels in human erythroblasts. Modulation by erythropoietin.

J Y Cheung, M B Elensky, U Brauneis, R C Scaduto Jr, L L Bell, D L Tillotson, and B A Miller

Department of Medicine, Milton S. Hershey Medical Center, Pennsylvania State University, Hershey 17033.

Find articles by Cheung, J. in: PubMed | Google Scholar

Department of Medicine, Milton S. Hershey Medical Center, Pennsylvania State University, Hershey 17033.

Find articles by Elensky, M. in: PubMed | Google Scholar

Department of Medicine, Milton S. Hershey Medical Center, Pennsylvania State University, Hershey 17033.

Find articles by Brauneis, U. in: PubMed | Google Scholar

Department of Medicine, Milton S. Hershey Medical Center, Pennsylvania State University, Hershey 17033.

Find articles by Scaduto, R. in: PubMed | Google Scholar

Department of Medicine, Milton S. Hershey Medical Center, Pennsylvania State University, Hershey 17033.

Find articles by Bell, L. in: PubMed | Google Scholar

Department of Medicine, Milton S. Hershey Medical Center, Pennsylvania State University, Hershey 17033.

Find articles by Tillotson, D. in: PubMed | Google Scholar

Department of Medicine, Milton S. Hershey Medical Center, Pennsylvania State University, Hershey 17033.

Find articles by Miller, B. in: PubMed | Google Scholar

Published November 1, 1992 - More info

Published in Volume 90, Issue 5 on November 1, 1992
J Clin Invest. 1992;90(5):1850–1856. https://doi.org/10.1172/JCI116061.
© 1992 The American Society for Clinical Investigation
Published November 1, 1992 - Version history
View PDF
Abstract

To investigate the mechanism of intracellular Ca2+ ([Cai]) increase in human burst-forming unit-erythroid-derived erythroblasts by erythropoietin, we measured [Cai] with digital video imaging, cellular phosphoinositides with high performance liquid chromatography, 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 Ca(2+)-activated K+ channel was detected in human erythroblasts. The magnitude of erythropoietin-induced [Cai] increase, however, was insufficient to open Ca(2+)-activated K+ channels. Our data suggest erythropoietin modulated a voltage-independent ion channel permeable to Ca2+, resulting in sustained increases in [Cai].

Browse pages

Click on an image below to see the page. View PDF of the complete article

icon of scanned page 1850
page 1850
icon of scanned page 1851
page 1851
icon of scanned page 1852
page 1852
icon of scanned page 1853
page 1853
icon of scanned page 1854
page 1854
icon of scanned page 1855
page 1855
icon of scanned page 1856
page 1856
Version history
  • Version 1 (November 1, 1992): No description

Article tools

  • View PDF
  • Download citation information
  • Send a comment
  • Terms of use
  • Standard abbreviations
  • Need help? Email the journal

Metrics

  • Article usage
  • Citations to this article

Go to

  • Top
  • Abstract
  • Version history
Advertisement
Advertisement

Copyright © 2025 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)

Sign up for email alerts