Go to JCI Insight
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Alerts
  • Advertising/recruitment
  • Subscribe
  • Contact
  • 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
    • Author's Takes
  • Reviews
    • View all reviews ...
    • 100th Anniversary of Insulin's Discovery (Jan 2021)
    • Hypoxia-inducible factors in disease pathophysiology and therapeutics (Oct 2020)
    • Latency in Infectious Disease (Jul 2020)
    • Immunotherapy in Hematological Cancers (Apr 2020)
    • Big Data's Future in Medicine (Feb 2020)
    • Mechanisms Underlying the Metabolic Syndrome (Oct 2019)
    • Reparative Immunology (Jul 2019)
    • View all review series ...
  • Viewpoint
  • Collections
    • Recently published
    • In-Press Preview
    • Commentaries
    • Concise Communication
    • Editorials
    • Viewpoint
    • Top read articles
  • Clinical Medicine
  • JCI This Month
    • Current issue
    • Past issues

  • Current issue
  • Past issues
  • Specialties
  • Reviews
  • Review series
  • Conversations with Giants in Medicine
  • Author's Takes
  • Recently published
  • In-Press Preview
  • Commentaries
  • Concise Communication
  • Editorials
  • Viewpoint
  • Top read articles
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Alerts
  • Advertising/recruitment
  • Subscribe
  • Contact
Top
  • View PDF
  • Download citation information
  • Send a letter
  • Share this article
  • Terms of use
  • Standard abbreviations
  • Need Help? E-mail the JCI
  • Top
  • Version history
  • Article usage
  • Citations to this article

Advertisement

Corrigendum Free access | 10.1172/JCI70656

GSK3β regulates physiological migration of stem/progenitor cells via cytoskeletal rearrangement

Kfir Lapid, Tomer Itkin, Gabriele D’Uva, Yossi Ovadya, Aya Ludin, Giulia Caglio, Alexander Kalinkovich, Karin Golan, Ziv Porat, Massimo Zollo, and Tsvee Lapidot

Find articles by Lapid, K. in: JCI | PubMed | Google Scholar

Find articles by Itkin, T. in: JCI | PubMed | Google Scholar

Find articles by D’Uva, G. in: JCI | PubMed | Google Scholar

Find articles by Ovadya, Y. in: JCI | PubMed | Google Scholar

Find articles by Ludin, A. in: JCI | PubMed | Google Scholar

Find articles by Caglio, G. in: JCI | PubMed | Google Scholar

Find articles by Kalinkovich, A. in: JCI | PubMed | Google Scholar

Find articles by Golan, K. in: JCI | PubMed | Google Scholar

Find articles by Porat, Z. in: JCI | PubMed | Google Scholar

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

Find articles by Lapidot, T. in: JCI | PubMed | Google Scholar

Published July 1, 2013 - More info

Published in Volume 123, Issue 7 on July 1, 2013
J Clin Invest. 2013;123(7):3183–3183. https://doi.org/10.1172/JCI70656.
© 2013 The American Society for Clinical Investigation
Published July 1, 2013 - Version history
View PDF

Related article:

GSK3β regulates physiological migration of stem/progenitor cells via cytoskeletal rearrangement
Kfir Lapid, … , Massimo Zollo, Tsvee Lapidot
Kfir Lapid, … , Massimo Zollo, Tsvee Lapidot
Research Article Hematology

GSK3β regulates physiological migration of stem/progenitor cells via cytoskeletal rearrangement

  • Text
  • PDF
Abstract

Regulation of hematopoietic stem and progenitor cell (HSPC) steady-state egress from the bone marrow (BM) to the circulation is poorly understood. While glycogen synthase kinase-3β (GSK3β) is known to participate in HSPC proliferation, we revealed an unexpected role in the preferential regulation of CXCL12-induced migration and steady-state egress of murine HSPCs, including long-term repopulating HSCs, over mature leukocytes. HSPC egress, regulated by circadian rhythms of CXCL12 and CXCR4 levels, correlated with dynamic expression of GSK3β in the BM. Nevertheless, GSK3β signaling was CXCL12/CXCR4 independent, suggesting that synchronization of both pathways is required for HSPC motility. Chemotaxis of HSPCs expressing higher levels of GSK3β compared with mature cells was selectively enhanced by stem cell factor–induced activation of GSK3β. Moreover, HSPC motility was regulated by norepinephrine and insulin-like growth factor-1 (IGF-1), which increased or reduced, respectively, GSK3β expression in BM HSPCs and their subsequent egress. Mechanistically, GSK3β signaling promoted preferential HSPC migration by regulating actin rearrangement and microtubuli turnover, including CXCL12-induced actin polarization and polymerization. Our study identifies a previously unknown role for GSK3β in physiological HSPC motility, dictating an active, rather than a passive, nature for homeostatic egress from the BM reservoir to the blood circulation.

Authors

Kfir Lapid, Tomer Itkin, Gabriele D’Uva, Yossi Ovadya, Aya Ludin, Giulia Caglio, Alexander Kalinkovich, Karin Golan, Ziv Porat, Massimo Zollo, Tsvee Lapidot

×

Original citation: J. Clin. Invest. 2013;123(4):1705–1717. doi:10.1172/JCI64149.

Citation for this erratum: J. Clin. Invest. 2013;123(7):3183. doi:10.1172/JCI70656.

Figure 3, B and C, was labeled incorrectly. The correct figure is below.

Figure 3

The authors regret the error.

Version history
  • Version 1 (July 1, 2013): No description

Article tools

  • View PDF
  • Download citation information
  • Send a letter
  • Share this article
  • Terms of use
  • Standard abbreviations
  • Need Help? E-mail the JCI

Metrics

  • Article usage
  • Citations to this article

Go to

  • Top
  • Version history
Advertisement
Advertisement
Follow JCI:
Copyright © 2021 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)

Sign up for email alerts