ArticleJournal of cellular physiology2004
Roles of stromal cell RANKL, OPG, and M-CSF expression in biphasic TGF-beta regulation of osteoclast differentiation.
Article in Journal of cellular physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 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.
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Who cites it
89 citing papers in PubMed, 185 citations in OpenAlex.
- A spatiotemporal atlas of senescence-associated secretory phenotype in fracture healing: stage-dependent mechanisms and therapeutic windows.Inflammation and regeneration · 2026Review
- Constitutive activation of TGF-β receptor type I promotes cortical and cancellous bone formation in adult mice.PloS one · 2026Article
- Macropinocytosis fuels osteoclast differentiation in bone-related diseases.Journal of orthopaedic translation · 2025Article
- Recent Advances in the Role of Osteocytes in Orthodontic Tooth Movement.International journal of molecular sciences · 2025Review
- Hydrothermal Magnesium Alloy Extracts Modulate MicroRNA Expression in RAW264.7 Cells: Implications for Bone Remodeling.Journal of functional biomaterials · 2025Article
- Bone remodelling after application of traction forces to the lumbar spine in women with chronic low back pain.Bone & joint research · 2025Article
- The Role of Cytokines in Orthodontic Tooth Movement.International journal of molecular sciences · 2025Review
- Matrix Metalloproteinase-9 Enhances Osteoclastogenesis: Insights from Transgenic Rabbit Bone Marrow Models and In Vitro Studies.International journal of molecular sciences · 2025Article
- Calcium Phosphates: A Key to Next-Generation In Vitro Bone Modeling.Advanced healthcare materials · 2024Review
- The balance between helper T 17 and regulatory T cells in osteoimmunology and relevant research progress on bone tissue engineering.Immunity, inflammation and disease · 2024Review
- Differential Gene Expression Involved in Bone Turnover of Mice Expressing Constitutively Active TGFβ Receptor Type I.International journal of molecular sciences · 2024Article
- Modulation of fracture healing by senescence-associated secretory phenotype (SASP): a narrative review of the current literature.European journal of medical research · 2024Review
- Targeting transforming growth factor beta signaling in metastatic osteosarcoma.Journal of bone oncology · 2023Review
- The Multifaceted Effects of Osteocytic TGFβ Signaling on the Skeletal and Extraskeletal Functions of Bone.Current osteoporosis reports · 2023Review
- Accelerated Bone Loss in Transgenic Mice Expressing Constitutively Active TGF-β Receptor Type I.International journal of molecular sciences · 2023Article
- Monocyte Differentiation on Atomic Layer-Deposited (ALD) Hydroxyapatite Coating on Titanium Substrate.Molecules (Basel, Switzerland) · 2023Article
- NF-κB Decoy ODN-Loaded Poly(Lactic-co-glycolic Acid) Nanospheres Inhibit Alveolar Ridge Resorption.International journal of molecular sciences · 2023Article
- One-Step Preparation of an Injectable Hydrogel Scaffold System Capable of Sequential Dual-Growth Factor Release to Maximize Bone Regeneration.Advanced healthcare materials · 2023Article
- The identification of hub-methylated differentially expressed genes in osteoarthritis patients is based on epigenomic and transcriptomic data.Frontiers in medicine · 2023Article
- Osteochondrogenesis by TGF-β3, BMP-2 and noggin growth factor combinations in anFrontiers in bioengineering and biotechnology · 2023Article
29 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
To better understand the complex roles of transforming growth factor-beta (TGF-beta) in bone metabolism, we examined the impact of a range of TGF-beta concentrations on osteoclast differentiation. In co-cultures of support cells and spleen or marrow osteoclast precursors, low TGF-beta concentrations stimulated while high concentrations inhibited differentiation. We investigated the influences of TGF-beta on macrophage colony stimulating factor (M-CSF), receptor activator of NF-kappaB ligand (RANKL), and osteoprotegerin (OPG) expression and found a dose dependent inhibition of M-CSF expression. RANKL expression was elevated at low TGF-beta concentrations with a less dramatic increase in OPG. Addition of OPG blocked differentiation at the stimulatory TGF-beta dose. Thus, low TGF-beta concentrations elevated the RANKL/OPG ratio while high concentrations did not, supporting that, at low TGF-beta concentrations, there is sufficient M-CSF and a high RANKL/OPG ratio to stimulate differentiation. At high TGF-beta concentrations, the RANKL/OPG ratio and M-CSF expression were both repressed and there was no differentiation. We examined whether TGF-beta-mediated repression of osteoclasts differentiation is due to these changes by adding M-CSF and/or RANKL and did not observe any impact on differentiation repression. We studied direct TGF-beta impacts on osteoclast precursors by culturing spleen or marrow cells with M-CSF and RANKL. TGF-beta treatment dose-dependently stimulated osteoclast differentiation. These data indicate that low TGF-beta levels stimulate osteoclast differentiation by impacting the RANKL/OPG ratio while high TGF-beta levels repress osteoclast differentiation by multiple avenues including mechanisms independent of the RANKL/OPG ratio or M-CSF expression regulation.
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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.