ArticleEndocrinology2014
Parathyroid hormone receptor signaling induces bone resorption in the adult skeleton by directly regulating the RANKL gene in osteocytes.
Article in Endocrinology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
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Who cites it
68 citing papers in PubMed, 113 citations in OpenAlex.
- Reprogramming bone homeostasis: The recoupling-oriented framework of bidirectional regulation strategies for osteoporosis.iScience · 2026Review
- Review
- Upregulation of Parathyroid Hormone Receptor 1 (International journal of molecular sciences · 2026Article
- Senescent Cells Involved in Deterioration of Bone Microstructure by High-Frequency Parathyroid Hormone 1-34 Administration and Bone Loss.Aging cell · 2026Article
- Heart Failure but Not Myocardial Infarction Is Causing Bone Loss in Rodent Models in an FGF23-Independent Manner.International journal of molecular sciences · 2025Article
- Immune-Guided Bone Healing: The Role of Osteoimmunity in Tissue Engineering Approaches.International journal of molecular sciences · 2025Review
- Advances in noninvasive diagnosis of renal osteodystrophy.Renal failure · 2025Review
- Administration of green tea polyphenols mitigates iron-overload-induced bone loss in a β-thalassemia mouse model.NPJ science of food · 2025Article
- Accelerated osteocytic citrate production in chronic kidney disease is associated with protection of the kidney.bioRxiv : the preprint server for biology · 2025Article
- CAV-1 regulates osteocyte communication with osteoclast and osteoblast precursors.Scientific reports · 2025Article
- High Dietary Phosphorus Impairs Bone Microarchitecture and Induces Alterations in the LGR4-R-Spondins Axis in Rats with Normal Renal Function.Nutrients · 2025Article
- Triglycerides-Total Cholesterol-Body Weight Index, bone metabolism indicators and bone mineral density in Chinese children: a mediation analysis.European journal of nutrition · 2025Observational
- CXCR4 is a response gene for parathyroid hormone which affects osteoblast and osteoclast function in vitro.Bone & joint research · 2025Article
- The antiosteoporotic effect of oxymatrine compared to testosterone in orchiectomized rats.Journal of orthopaedic surgery and research · 2025Article
- Computational simulations of endocrine bone diseases related to pathological glandular PTH secretion using a multi-scale bone cell population model.Frontiers in bioengineering and biotechnology · 2025Article
- Clinical Utility of Bone Turnover Markers in Chronic Kidney Disease.Journal of bone metabolism · 2024Article
- Bone Disease in Primary Hyperparathyroidism-Changes Occurring in Bone Metabolism and New Potential Treatment Strategies.International journal of molecular sciences · 2024Review
- RANKL, but Not R-Spondins, Is Involved in Vascular Smooth Muscle Cell Calcification through LGR4 Interaction.International journal of molecular sciences · 2024Article
- Review
- Inhibition of RANKL improves the skeletal phenotype of adenine-induced chronic kidney disease in mice.JBMR plus · 2024Article
8 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
PTH upregulates the expression of the receptor activator of nuclear factor κB ligand (Rankl) in cells of the osteoblastic lineage, but the precise differentiation stage of the PTH target cell responsible for RANKL-mediated stimulation of bone resorption remains undefined. We report that constitutive activation of PTH receptor signaling only in osteocytes in transgenic mice (DMP1-caPTHR1) was sufficient to increase Rankl expression and bone resorption. Resorption in DMP1-caPTHR1 mice crossed with mice lacking the distal control region regulated by PTH in the Rankl gene (DCR(-/-)) was similar to DMP1-caPTHR1 mice at 1 month of age, but progressively declined to reach values undistinguishable from wild-type (WT) mice at 5 months of age. Moreover, DMP1-caPTHR1 mice exhibited low tissue material density and increased serum alkaline phosphatase activity at 5 month of age, and these indices of high remodeling were partially and totally corrected in compound DMP1-caPTHR1;DCR(-/-) male mice, and less affected in female mice. Rankl expression in bones from DMP1-caPTHR1 mice was elevated at both 1 and 5 months of age, whereas it was high, similar to DMP1-caPTHR1 mice at 1 month, but low, similar to WT levels at 5 months in compound mice. Moreover, PTH increased Rankl and decreased Sost and Opg expression in ex vivo bone organ cultures established from WT mice, but only regulated Sost and Opg expression in cultures from DCR(-/-) mice. PTH also increased RANKL expression in osteocyte-containing primary cultures of calvarial cells, in isolated murine osteocytes, and in WT but not in DCR(-/-) osteocyte-enriched bones. Thus, PTH upregulates Rankl expression in osteocytes in vitro, ex vivo and in vivo, and resorption induced by PTH receptor signaling in the adult skeleton requires direct regulation of the Rankl gene in osteocytes.
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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.