ArticleThe Journal of biological chemistry2009
Commitment to the osteoblast lineage is not required for RANKL gene expression.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 51 citations in OpenAlex.
- Interleukin-34 orchestrates bone formation through its binding to bone morphogenic proteins.Theranostics · 2025Article
- The hypertrophic chondrocyte: To be or not to be.Histology and histopathology · 2021Review
- Effects of Extracellular Osteoanabolic Agents on the Endogenous Response of Osteoblastic Cells.Cells · 2021Review
- Osteoimmunology.Cold Spring Harbor perspectives in medicine · 2019Review
- Parathyroid hormone(1-34) and its analogs differentially modulate osteoblasticThe Journal of biological chemistry · 2018Article
- Article
- Parathyroid Hormone Signaling in Osteocytes.JBMR plus · 2018Review
- The Modulatory Effects of Mesenchymal Stem Cells on Osteoclastogenesis.Stem cells international · 2016Review
- RANKL/OPG; Critical role in bone physiology.Reviews in endocrine & metabolic disorders · 2015Review
- The osteocyte: key player in regulating bone turnover.RMD open · 2015Review
- Osteocyte control of bone remodeling: is sclerostin a key molecular coordinator of the balanced bone resorption-formation cycles?Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2014Review
- Article
- Serotonin: a novel bone mass controller may have implications for alveolar bone.Journal of negative results in biomedicine · 2013Article
- Osteocyte control of osteoclastogenesis.Bone · 2013Review
- MKP-1 is essential for canonical vitamin D-induced signaling through nuclear import and regulates RANKL expression and function.Molecular endocrinology (Baltimore, Md.) · 2012Article
- Osteocyte RANKL: new insights into the control of bone remodeling.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2012Review
- Direct recruitment of polycomb repressive complex 1 to chromatin by core binding transcription factors.Molecular cell · 2012Article
- Matrix-embedded cells control osteoclast formation.Nature medicine · 2011Article
- Decreased oxidative stress and greater bone anabolism in the aged, when compared to the young, murine skeleton with parathyroid hormone administration.Aging cell · 2010Article
- Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Differentiation of bone-resorbing osteoclasts from hematopoietic precursors depends upon expression of the cytokine receptor activator of NFkappaB ligand (RANKL) by fibroblastic stromal cells, which some evidence suggests are of the osteoblast lineage. We have shown previously that hormonal-responsiveness of the murine RANKL gene is mediated in part by a distal enhancer that binds Runx2, a transcription factor required for commitment to the osteoblast lineage, supporting the idea that osteoclast-supporting stromal cells may be osteoblasts or their progenitors. However, in this study we demonstrate that parathyroid hormone (PTH) stimulation of RANKL in mice is not affected by a significant reduction in the number of osteoblasts. Consistent with this, neither Runx2, nor Cbfb, a binding partner essential for Runx activity, are required for basal or PTH-stimulated RANKL expression in fibroblastic stromal cell models. Nonetheless, RANKL responsiveness to PTH was elevated in cultured calvaria cells expressing high levels of osterix, another transcription factor required for osteoblast differentiation, and this was associated with elevated PTH receptor expression. The responsiveness of RANKL to 1,25-dihydroxyvitamin D(3) was not elevated in the osterix-expressing cells. Together, these results suggest that commitment to the osteoblast lineage is not a requirement for RANKL gene transcription in fibroblastic stromal cells but may enhance responsiveness of this gene to specific hormones via control of their receptors.
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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.