ArticleThe Journal of biological chemistry2010
TRPV-5 mediates a receptor activator of NF-kappaB (RANK) ligand-induced increase in cytosolic Ca2+ in human osteoclasts and down-regulates bone resorption.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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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
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.
- Metaanalysis Reveals Genetic Correlates of Osteoporosis Pathogenesis.The Journal of rheumatology · 2021Pooled it
- Dual Osteoprotective Actions of the Kefir Peptide KFP-1: Enhancement of Bone Formation and Suppression of Bone Resorption in Cells and Murine Models.Calcified tissue international · 2026Article
- The role of calcium ions and the transient receptor potential vanilloid (TRPV) channel in bone remodelling and orthodontic tooth movement.Molecular biology reports · 2025Review
- The role of transient receptor potential channels in chronic kidney disease-mineral and bone disorder.Frontiers in pharmacology · 2025Review
- Review
- Ion channels in osteoarthritis: emerging roles and potential targets.Nature reviews. Rheumatology · 2024Review
- The role of calcium channels in osteoporosis and their therapeutic potential.Frontiers in endocrinology · 2024Review
- Alterations in the microenvironment and the effects produced of TRPV5 in osteoporosis.Journal of translational medicine · 2023Review
- Calcium-Permeable Channels Cooperation for Rheumatoid Arthritis: Therapeutic Opportunities.Biomolecules · 2022Review
- Article
- The role of TRPV channels in osteoporosis.Molecular biology reports · 2022Review
- TRPV6 is a potential regulator of bone resorption in bone loss induced by estrogen deficiency.iScience · 2021Article
- Purification and Biological Function of Caldecrin.Medicines (Basel, Switzerland) · 2021Review
- Finely-Tuned Calcium Oscillations in Osteoclast Differentiation and Bone Resorption.International journal of molecular sciences · 2020Review
- The Role of CaInternational journal of molecular sciences · 2020Review
- Icariin Promotes Fracture Healing in Ovariectomized Rats.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Physalin D inhibits RANKL-induced osteoclastogenesis and bone loss via regulating calcium signaling.BMB reports · 2020Article
- Calcium Homeostasis: A Potential Vicious Cycle of Bone Metastasis in Breast Cancers.Frontiers in oncology · 2020Review
- The Role of Calcium-Calcineurin-NFAT Signaling Pathway in Health and Autoimmune Diseases.Frontiers in immunology · 2020Review
- Regulation of TRPV5 transcription and expression by E2/ERα signalling contributes to inhibition of osteoclastogenesis.Journal of cellular and molecular medicine · 2018Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Most of the signaling effectors located downstream of receptor activator of NF-kappaB (RANK) activation are calcium-sensitive. However, the early signaling events that lead to the mobilization of intracellular calcium in human osteoclasts are still poorly understood. The Ca(2+)-sensitive fluorescent probe Fura2 was used to detect changes in the intracellular concentration of Ca(2+) ([Ca(2+)](i)) in a model of human osteoclasts. Stimulating these cells with receptor activator of NF-kappaB ligand (RANKL) induced a rapid and significant increase in [Ca(2+)](i). Adding extracellular Ca(2+) chelators, depleting intracellular stores, and the use of a phospholipase C inhibitor all indicated that the Ca(2+) was of extracellular origin, suggesting the involvement of a Ca(2+) channel. We showed that none of the classical Ca(2+) channels (L-, T-, or R-type) were involved in the RANKL-induced Ca(2+) spike. However, the effect of high doses of Gd(3+) did suggest that TRP family channels were present in human osteoclasts. The TRPV-5 channel was expressed in osteoclasts and was mainly located in the cellular area in contact with the bone surface. Furthermore, the RNA inactivation of TRPV-5 channel completely inhibited the RANKL-induced increase in [Ca(2+)](i), which was accompanied in the long term by marked activation of bone resorption. Overall, our results show that RANKL induced a significant increase in [Ca(2+)](i) of extracellular origin, probably as a result of the opening of TRPV-5 calcium channels on the surface of human osteoclasts. Our findings suggest that TRPV-5 contributes to maintaining the homeostasis of the human skeleton via a negative feedback loop in RANKL-induced bone resorption.
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Registered trials
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