ArticleScientific reports2018
Glucocorticoids suppress Wnt16 expression in osteoblasts in vitro and in vivo.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 45 citations in OpenAlex.
- The influence of hormonal changes during pregnancy on bone metabolism - a mini review.Frontiers in endocrinology · 2026Review
- Wnt16: a new potential therapeutic target for osteoporotic non-vertebral fracture treatment.Frontiers in aging · 2026Review
- The therapeutic potential of descending regulatory pathways from brain to bone in osteoporosis: focusing on the brain-bone axis.Frontiers in endocrinology · 2026Review
- Disrupted Osteoblastogenesis and Mitochondrial Remodeling in MSCs from Patients with Cushing's Syndrome.Stem cell reviews and reports · 2025Article
- Beyond Bone Loss: A Biology Perspective on Osteoporosis Pathogenesis, Multi-Omics Approaches, and Interconnected Mechanisms.Biomedicines · 2025Review
- Reducing PDK4 level constitutes a pivotal mechanism for glucocorticoids to impede osteoblastic differentiation through the enhancement of ferroptosis in mesenchymal stem cells.Stem cell research & therapy · 2025Article
- Article
- Decreasing miR-433-3p Activity in the Osteoblast Lineage Blunts Glucocorticoid-mediated Bone Loss.Endocrinology · 2025Article
- Antiresorptive effect of a semisynthetic triterpene from Combretum leprosum Mart. on dexamethasone-induced osteoporosis in rats.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2025Article
- Protein kinase G2 activation restores Wnt signaling and bone mass in glucocorticoid-induced osteoporosis in mice.JCI insight · 2024Article
- The Therapeutic Potential of Two Egyptian Plant Extracts for Mitigating Dexamethasone-Induced Osteoporosis in Rats: Nrf2/HO-1 and RANK/RANKL/OPG Signals.Antioxidants (Basel, Switzerland) · 2024Article
- Local Effects of Steroid Hormones within the Bone Microenvironment.International journal of molecular sciences · 2023Review
- Genetic Variants in WNT16 and PKD2L1 Locus Affect Heel Ultrasound Bone Stiffness: Analyses from the General Population and Patients Evaluated for Osteoporosis.Calcified tissue international · 2023Article
- Management of Adrenal Cortical Adenomas: Assessment of Bone Status in Patients with (Non-Functioning) Adrenal Incidentalomas.Journal of clinical medicine · 2023Review
- Laponite intercalated biomimetic multilayer coating prevents glucocorticoids induced orthopedic implant failure.Bioactive materials · 2023Article
- Pathogenic mechanisms of glucocorticoid-induced osteoporosis.Cytokine & growth factor reviews · 2023Review
- Molecular Hydrogen Prevents Osteoclast Activation in a Glucocorticoid-Induced Osteoporosis Zebrafish Scale Model.Antioxidants (Basel, Switzerland) · 2023Article
- Inhibition of Cdk5 Ameliorates Skeletal Bone Loss in Glucocorticoid-Treated Mice.Biomedicines · 2022Article
- Effects of Alendronate and Dexamethasone on Osteoclast Gene Expression and Bone Resorption in Mouse Marrow Cultures.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2022Article
- Wnt16 signaling in bone homeostasis and osteoarthristis.Frontiers in endocrinology · 2022Review
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glucocorticoid-induced osteoporosis is a frequent complication of systemic glucocorticoid (GC) therapy and mainly characterized by suppressed osteoblast activity. Wnt16 derived from osteogenic cells is a key determinant of bone mass. Here, we assessed whether GC suppress bone formation via inhibiting Wnt16 expression. GC treatment with dexamethasone (DEX) decreased Wnt16 mRNA levels in murine bone marrow stromal cells (mBMSCs) time- and dose-dependently. Similarly, Wnt16 expression was also suppressed after DEX treatment in calvarial organ cultures. Consistently, mice receiving GC-containing slow-release prednisolone pellets showed lower skeletal Wnt16 mRNA levels and bone mineral density than placebo-treated mice. The suppression of Wnt16 by GCs was GC-receptor-dependent as co-treatment of mBMSCs with DEX and the GR antagonist RU-486 abrogated the GC-mediated suppression of Wnt16. Likewise, DEX failed to suppress Wnt16 expression in GR knockout-mBMSCs. In addition, Wnt16 mRNA levels were unaltered in bone tissue of GC-treated GR dimerization-defective GR
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