ArticleJournal of molecular histology2021
Prednisolone induces osteocytes apoptosis by promoting Notum expression and inhibiting PI3K/AKT/GSK3β/β-catenin pathway.
Article in Journal of molecular histology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 32 citations in OpenAlex.
- Discovery of anthraquinones as potent Notum inhibitors for treating osteoporosis by integrating biochemical, phytochemical, computational, and experimental assays.Journal of pharmaceutical analysis · 2026Article
- NOTUM Enhances Cartilage Repair via Wnt/β-Catenin Modulation in a Rabbit Osteochondral Defect Model.International journal of molecular sciences · 2026Article
- The therapeutic potential of descending regulatory pathways from brain to bone in osteoporosis: focusing on the brain-bone axis.Frontiers in endocrinology · 2026Review
- Selenium Attenuates Dexamethasone-Induced Osteoblast Dysfunction and Prevents Femoral Head Osteonecrosis via PI3K/AKT/GSK3β Pathway Activation.Orthopaedic surgery · 2025Article
- High-efficient discovering the potent anti-Notum agents from herbal medicines for combating glucocorticoid-induced osteoporosis.Acta pharmaceutica Sinica. B · 2025Article
- Review
- Impact of short and long-term application of low-level laser therapy on mandibular alveolar process of osteoporotic rats - a Histological and Molecular Study.Lasers in medical science · 2025Article
- The central mechanotransducer in osteoporosis pathogenesis and therapy.Frontiers in endocrinology · 2025Review
- New mechanistic understanding of osteoclast differentiation and bone resorption mediated by P2X7 receptors and PI3K-Akt-GSK3β signaling.Cellular & molecular biology letters · 2024Article
- Metformin Modulates Cell Oxidative Stress to Mitigate Corticosteroid-Induced Suppression of Osteogenesis in a 3D Model.Journal of inflammation research · 2024Article
- The effect of Rutin hydrate on Glucocorticoids induced osteoporosis in mandibular alveolar bone in Albino rats (Radiological, histological and histochemical study).The Saudi dental journal · 2022Article
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
The apoptosis of mature osteocytes is the main factor causing damage to the microstructure of cortical bone in glucocorticoid-induced osteoporosis (GIOP). Our previous research found damaged areas and empty osteocytes lacunae in the tibial cortical bone of GIOP mice. However, the specific mechanism has not been clarified. Recently, a study showed that the quality of the cortical bone significantly increased by knocking out Notum, a gene encoding α/β hydrolase. However, it is not clear whether Notum affects cortical bone remodeling by participating in glucocorticoids (GCs)-induced apoptosis of osteocytes. The present study aimed to explore the correlation between Notum, osteocytes apoptosis, and cortical bone quality in GIOP. Prednisolone acetate was intragastrically administered to mice for two weeks. Histochemical staining was applied to evaluate changes in GIOP and Notum expression. Osteocytes were stimulated with prednisolone, and cell viability was assessed via CCK8. Hoechst 33342/PI staining, flow cytometry, RT-PCR, and western blot were used to detect osteocytes apoptosis, siRNA transfection efficiency, and expressions of pathway related factors. The results showed that the number of empty osteocytes lacunae increased in GIOP mice. TUNEL-stained apoptotic osteocytes and Notum immuno-positive osteocytes were also observed. Furthermore, prednisolone was found to promote Notum expression and osteocytes apoptosis in vitro. Knocking down Notum via siRNA partially restored osteocytes apoptosis and phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/glycogen synthase kinase-3β (GSK3β)/β-catenin pathway. These findings showed GCs-induced osteocytes apoptosis by promoting Notum expression and inhibiting PI3K/AKT/GSK3β/β-catenin pathway. Thus, Notum might be a potential therapeutic target for the treatment of GIOP.
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