ArticleJournal of cellular biochemistry2011
Physical and functional interactions between Runx2 and HIF-1α induce vascular endothelial growth factor gene expression.
Article in Journal of cellular biochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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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
58 citing papers in PubMed, 97 citations in OpenAlex.
- VEGFA is essential for the potentiation of ATRA on BMP9-induced osteogenesis of preadipocytes and osteoporotic fracture healing.In vitro cellular & developmental biology. Animal · 2026Article
- AMPK/mTORC2/AKT-473/RUNX2 signaling axis modulates epithelial-mesenchymal transition and bone tropism in breast cancer.Frontiers in oncology · 2026Article
- Overexpression of RUNX2 promotes breast cancer multi-organ metastasis through stabilizing c-Myc.Cell death & disease · 2025Article
- Molecular Crosstalk Between RUNX2 and HIF-1α in Osteosarcoma: Implications for Angiogenesis, Metastasis, and Therapy Resistance.International journal of molecular sciences · 2025Review
- In-silico analysis predicts disruption of normal angiogenesis as a causative factor in osteoporosis pathogenesis.BMC genomic data · 2024Article
- Placental Tissue Calcification and Its Molecular Pathways in Female Patients with Late-Onset Preeclampsia.Biomolecules · 2024Article
- Article
- RUNX transcription factors: biological functions and implications in cancer.Clinical and experimental medicine · 2024Review
- Mesenchymal stem cell-derived exosomes enriched with miR-218 reduce the epithelial-mesenchymal transition and angiogenesis in triple-negative breast cancer cells.European journal of medical research · 2023Article
- Insights on the role of L-lactate as a signaling molecule in skin aging.Biogerontology · 2023Review
- Recent Advances in Bioengineering Bone Revascularization Based on Composite Materials Comprising Hydroxyapatite.International journal of molecular sciences · 2023Review
- GRP78 promotes the osteogenic and angiogenic response in periodontal ligament stem cells.European cells & materials · 2023Article
- Review
- Review
- Pro-Calcific Environment Impairs Ischaemia-Driven Angiogenesis.International journal of molecular sciences · 2022Article
- A New Perspective for Bone Tissue Engineering: Human Mesenchymal Stromal Cells Well-Survive Cryopreservation on β-TCP Scaffold and Show Increased Ability for Osteogenic Differentiation.International journal of molecular sciences · 2022Article
- Regulatory Role of the RUNX2 Transcription Factor in Lung Cancer Apoptosis.International journal of cell biology · 2022Article
- HIF-1α in Osteoarthritis: From Pathogenesis to Therapeutic Implications.Frontiers in pharmacology · 2022Review
- Runx1 protects against the pathological progression of osteoarthritis.Bone research · 2021Article
- Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
Abstract
Angiogenesis and bone formation are intimately related processes. Hypoxia during early bone development stabilizes hypoxia-inducible factor-1α (HIF-1α) and increases angiogenic signals including vascular endothelial growth factor (VEGF). Furthermore, stabilization of HIF-1α by genetic or chemical means stimulates bone formation. On the other hand, deficiency of Runx2, a key osteogenic transcription factor, prevents vascular invasion of bone and VEGF expression. This study explores the possibility that HIF-1α and Runx2 interact to activate angiogenic signals. Runx2 over-expression in mesenchymal cells increased VEGF mRNA and protein under both normoxic and hypoxic conditions. In normoxia, Runx2 also dramatically increased HIF-1α protein. In all cases, the Runx2 response was inhibited by siRNA-mediated suppression of HIF-1α and completely blocked by the HIF-1α inhibitor, echinomycin. Similarly, treatment of preosteoblast cells with Runx2 siRNA reduced VEGF mRNA in normoxia or hypoxia. However, Runx2 is not essential for the HIF-1α response since VEGF is induced by hypoxia even in Runx2-null cells. Endogenous Runx2 and HIF-1α were colocalized to the nuclei of MC3T3-E1 preosteoblast cells. Moreover, HIF-1α and Runx2 physically interact using sites within the Runx2 RUNT domain. Chromatin immunoprecipitation also provided evidence for colocalization of Runx2 and HIF-1α on the VEGF promoter. In addition, Runx2 stimulated HIF-1α-dependent activation of an HRE-luciferase reporter gene without requiring a separate Runx2-binding enhancer. These studies indicate that Runx2 functions together with HIF-1α to stimulate angiogenic gene expression in bone cells and may in part explain the known requirement for Runx2 in bone vascularization.
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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.