ArticleThe Journal of clinical investigation2013
GSK3β regulates physiological migration of stem/progenitor cells via cytoskeletal rearrangement.
Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 37 citations in OpenAlex.
- Circadian control of immune homeostasis in cardiovascular health and disease.Frontiers in immunology · 2026Review
- Stem Cells Run Like Clockwork for Stroke Therapeutics.Stem cell reviews and reports · 2025Article
- Drug-eluting intraocular lens with sustained bromfenac release for conquering posterior capsular opacification.Bioactive materials · 2022Article
- Review
- Effects of signaling pathway inhibitors on hematopoietic stem cells.Molecular medicine reports · 2021Article
- Review
- MicroRNAs in the Migration of Mesenchymal Stem Cells.Stem cell reviews and reports · 2019Review
- MCP-1-induced ERK/GSK-3β/Snail signaling facilitates the epithelial-mesenchymal transition and promotes the migration of MCF-7 human breast carcinoma cells.Cellular & molecular immunology · 2017Article
- Delayed treatment of 6-Bromoindirubin-3'-oxime stimulates neurogenesis and functional recovery after focal ischemic stroke in mice.International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience · 2017Article
- GSK3β mediates pancreatic cancer cell invasion in vitro via the CXCR4/MMP-2 Pathway.Cancer cell international · 2015Article
- Carbon monoxide down-regulates α4β1 integrin-specific ligand binding and cell adhesion: a possible mechanism for cell mobilization.BMC immunology · 2014Article
- Glycogen synthase kinase-3β inhibition depletes the population of prostate cancer stem/progenitor-like cells and attenuates metastatic growth.Oncotarget · 2014Article
- Reactive oxygen species regulate hematopoietic stem cell self-renewal, migration and development, as well as their bone marrow microenvironment.Antioxidants & redox signaling · 2014Review
- Single-cell technologies sharpen up mammalian stem cell research.Nature cell biology · 2014Review
- Cellular complexity of the bone marrow hematopoietic stem cell niche.Calcified tissue international · 2014Review
- A major role for RCAN1 in atherosclerosis progression.EMBO molecular medicine · 2013Article
- Dynamic Cross Talk between S1P and CXCL12 Regulates Hematopoietic Stem Cells Migration, Development and Bone Remodeling.Pharmaceuticals (Basel, Switzerland) · 2013Article
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.