ArticleJournal of cellular and molecular medicine2018
Regulation of TRPV5 transcription and expression by E2/ERα signalling contributes to inhibition of osteoclastogenesis.
Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- Estrous cycle modulates fasting-induced torpor propensity via hypothalamic estrogen signalling.Scientific reports · 2026Article
- Circadian regulation of osteoclast lysosomal-resorption machinery: implications for osteoporosis therapy.Frontiers in cell and developmental biology · 2026Review
- The role of calcium ions and the transient receptor potential vanilloid (TRPV) channel in bone remodelling and orthodontic tooth movement.Molecular biology reports · 2025Review
- Osteoinductive micro-nano guided bone regeneration membrane for in situ bone defect repair.Stem cell research & therapy · 2024Article
- Bone equilibria and disruptions.Journal of the Pediatric Orthopaedic Society of North America · 2024Article
- 24-h Urinary Calcium Excretion and Renal Outcomes in Hospitalized Patients with and without Chronic Kidney Disease.Journal of clinical medicine · 2023Article
- Alterations in the microenvironment and the effects produced of TRPV5 in osteoporosis.Journal of translational medicine · 2023Review
- Intracellular Helix-Loop-Helix Domain Modulates Inactivation Kinetics of Mammalian TRPV5 and TRPV6 Channels.International journal of molecular sciences · 2023Article
- The recent progress of endocrine therapy-induced osteoporosis in estrogen-positive breast cancer therapy.Frontiers in oncology · 2023Review
- Calcium-Permeable Channels Cooperation for Rheumatoid Arthritis: Therapeutic Opportunities.Biomolecules · 2022Review
- TRPV6 is a potential regulator of bone resorption in bone loss induced by estrogen deficiency.iScience · 2021Article
- The calcium channel TRPV6 is a novel regulator of RANKL-induced osteoclastic differentiation and bone absorption activity through the IGF-PI3K-AKT pathway.Cell proliferation · 2021Article
- Steroids and TRP Channels: A Close Relationship.International journal of molecular sciences · 2020Review
- The Role of CaInternational journal of molecular sciences · 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
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The increasing of osteoclasts formation and activity because of oestrogen (E2) deficiency is very important in the aetiology of postmenopausal osteoporosis. Our previous studies showed that E2 inhibited osteoclastic bone resorption by increasing the expression of Transient Receptor Potential Vanilloid 5 (TRPV5) channel. However, the exact mechanism by which E2 increases TRPV5 expression is not fully elucidated. In this study, Western blot, quantitative real-time PCR, tartrate-resistant acid phosphatase staining, F-actin ring staining, chromatin immunoprecipitation and luciferase assay were applied to explore the mechanisms that E2-induced TRPV5 expression contributes to the inhibition of osteoclastogenesis. The results showed that silencing or overexpressing of TRPV5 significantly affected osteoclasts differentiation and activity. Silencing of TRPV5 obviously alleviated E2-inhibited osteoclastogenesis, resulting in increasing of bone resorption. E2 stimulated mature osteoclasts apoptosis by increasing TRPV5 expression. Further studies showed that E2 increased TRPV5 expression through the interaction of the oestrogen receptor α (ERα) with NF-κB, which could directly bind to the fragment of -286 nt ~ -277 nt in the promoter region of trpv5. Taken together, we conclude that TRPV5 plays a dominant effect in E2-mediated osteoclasts formation, bone resorption activity and osteoclasts apoptosis. Furthermore, NF-κB plays an important role in the transcriptional activation of E2-ERα stimulated TRPV5 expression.
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