ArticleJournal of cellular physiology2017
Estrogens and androgens inhibit association of RANKL with the pre-osteoblast membrane through post-translational mechanisms.
Article in Journal of cellular physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
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- Exploring the Interaction Between Sjögren's Syndrome and Osteoporosis: Pathophysiological Mechanisms and Management Strategies.International journal of general medicine · 2025Review
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- Sex-Related Differences in the Pathophysiology, Cardiac Imaging, and Clinical Outcomes of Aortic Stenosis: A Narrative Review.Journal of clinical medicine · 2024Review
- Associations of Hormonal and Metabolic Parameters with Bone Mineralization in Young Adult Females.Nutrients · 2023Article
- Associations of Bone Mineral Density with RANKL and Osteoprotegerin in Arab Postmenopausal Women: A Cross-Sectional Study.Medicina (Kaunas, Lithuania) · 2022Article
- Mechanisms and Future of Non-Small Cell Lung Cancer Metastasis.Frontiers in oncology · 2020Review
- Influences of Sex and Estrogen in Arterial and Valvular Calcification.Frontiers in endocrinology · 2019Review
- Roles of the RANKL-RANK axis in antitumour immunity - implications for therapy.Nature reviews. Clinical oncology · 2018Review
- Estrogens and selective estrogen receptor modulators differentially antagonize Runx2 in ST2 mesenchymal progenitor cells.The Journal of steroid biochemistry and molecular biology · 2018Article
- Communication between genomic and non-genomic signaling events coordinate steroid hormone actions.Steroids · 2018Article
- MiR-23a targets RUNX2 and suppresses ginsenoside Rg1-induced angiogenesis in endothelial cells.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 3 countries.
Funding
Abstract
We have recently demonstrated that RUNX2 promoted, and 17β-Estradiol (E2) diminished, association of RANKL with the cell membrane in pre-osteoblast cultures. Here we show that, similar to E2, dihydrotestosterone (DHT) diminishes association of RANKL, and transiently transfected GFP-RANKL with the pre-osteoblast membrane without decreasing total RANKL mRNA or protein levels. Diminution of membrane-associated RANKL was accompanied with marked suppression of osteoclast differentiation from co-cultured pre-osteoclasts, even though DHT increased, not decreased, RANKL concentrations in pre-osteoblast conditioned media. A marked decrease in membrane-associated RANKL was observed after 30 min of either E2 or DHT treatment, and near-complete inhibition was observed by 1 hr, suggesting that the diminution of RANKL membrane association was mediated through non-genomic mechanisms. Further indicating dispensability of nuclear action of estrogen receptor, E2-mediated inhibition of RANKL membrane association was mimicked by an estrogen dendrimer conjugate (EDC) that cannot enter the cell nucleus. Finally, the inhibitory effect of E2 and DHT on RANKL membrane association was counteracted by the MMP inhibitor NNGH, and the effect of E2 (and not DHT) was antagonized by the Src inhibitor SU6656. Taken together, these results suggest that estrogens and androgens inhibit osteoblast-driven osteoclastogenesis through non-genomic mechanism(s) that entail, MMP-mediated RANKL dissociation from the cell membrane.
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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.