ArticleBlood advances2019
HIF prolyl hydroxylase inhibitor FG-4497 enhances mouse hematopoietic stem cell mobilization via VEGFR2/KDR.
Article in Blood advances, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- Comparison of the efficacy of hematopoietic stem cell mobilization regimens: a systematic review and network meta-analysis of preclinical studies.Stem cell research & therapy · 2021Pooled it
- Natural extract-derived compounds for the treatment of hematological diseases through modulation of the bone marrow microenvironment.Frontiers in chemistry · 2026Review
- Preliminary delivery efficiency prediction of nanotherapeutics into crucial cell populations in bone marrow niche.Asian journal of pharmaceutical sciences · 2023Article
- Platelet-derived circulating soluble P-selectin is sufficient to induce hematopoietic stem cell mobilization.Stem cell research & therapy · 2023Article
- Cell-intrinsic factors governing quiescence vis-à-vis activation of adult hematopoietic stem cells.Molecular and cellular biochemistry · 2023Review
- Evaluation of potential miRNA sponge effects of SARS genomes in human.Non-coding RNA research · 2022Article
- JMJD6 promotes self-renewal and regenerative capacity of hematopoietic stem cells.Blood advances · 2021Article
- Hypoxia, HIF-1α, and COVID-19: from pathogenic factors to potential therapeutic targets.Acta pharmacologica Sinica · 2020Review
- Collection and Processing of Mobilized Mouse Peripheral Blood at Lowered Oxygen Tension Yields Enhanced Numbers of Hematopoietic Stem Cells.Stem cell reviews and reports · 2020Article
- Bacterial Lipopolysaccharides Suppress Erythroblastic Islands and Erythropoiesis in the Bone Marrow in an Extrinsic and G- CSF-, IL-1-, and TNF-Independent Manner.Frontiers in immunology · 2020Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In normoxia, hypoxia-inducible transcription factors (HIFs) are rapidly degraded within the cytoplasm as a consequence of their prolyl hydroxylation by oxygen-dependent prolyl hydroxylase domain (PHD) enzymes. We have previously shown that hematopoietic stem and progenitor cells (HSPCs) require HIF-1 for effective mobilization in response to granulocyte colony-stimulating factor (G-CSF) and CXCR4 antagonist AMD3100/plerixafor. Conversely, HIF PHD inhibitors that stabilize HIF-1 protein in vivo enhance HSPC mobilization in response to G-CSF or AMD3100 in a cell-intrinsic manner. We now show that extrinsic mechanisms involving vascular endothelial growth factor receptor-2 (VEGFR2), via bone marrow (BM) endothelial cells, are also at play. PTK787/vatalanib, a tyrosine kinase inhibitor selective for VEGFR1 and VEGFR2, and neutralizing anti-VEGFR2 monoclonal antibody DC101 blocked enhancement of HSPC mobilization by FG-4497. VEGFR2 was absent on mesenchymal and hematopoietic cells and was detected only in Sca1
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