ArticleCell death & disease2013
Dexamethasone shifts bone marrow stromal cells from osteoblasts to adipocytes by C/EBPalpha promoter methylation.
Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers.
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Who cites it
109 citing papers in PubMed, 175 citations in OpenAlex.
- The miR-212-3p/transferrin axis promotes bone regeneration by modulating iron homeostasis through Schwann cell Exosome-BMSCs communication.Bioactive materials · 2026Article
- Epigenetic regulatory networks in the pathogenesis and treatment of osteoporosis subtypes.Molecular biomedicine · 2026Review
- Dexamethasone-mediated modulation of the renin-angiotensin system: current insights.Pharmacological reports : PR · 2026Review
- Bone Marrow Adipocytes in Multiple Myeloma: Emerging Immunometabolic Interactions and Implications for Immunotherapy.Cancers · 2026Review
- Homocysteine-induced bone formation dysfunction reversed by icariin via the AKT/FOXO1 signaling pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Dysregulation of the MACF1-Rab14/KIF16B-FGFR Vesicular Trafficking Axis Skews MSC Lineage Commitment in Glucocorticoid-Induced Osteoporosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Wubi Shanyao Pills ameliorate glucocorticoid-induced osteoporosis by regulating bone marrow T cell homing as an immune intermediate to restore bone metabolism.Chinese medicine · 2026Article
- Berberine Attenuates Glucocorticoid-Induced Bone Loss in Mice: Associated with the Gut Microbiota-Glycerophospholipid Metabolic Axis.Foods (Basel, Switzerland) · 2026Article
- Advances in the mechanism for steroid-induced osteonecrosis of the femoral head.Bone research · 2026Review
- Ceria nanoparticles guard against glucocorticoid induced bone homeostasis imbalance through the promotion of osteogenesis and inhibition of osteoclastogenesis.Materials today. Bio · 2025Article
- The N-butanol extract of modified Yanghe decoction alleviates ferroptosis in bone marrow mesenchymal stem cells in glucocorticoid-induced osteoporosis by activating the HIF-1α/GPX4 signaling pathway.Journal of orthopaedic surgery and research · 2025Article
- Review
- Repurposed Drugs for Heterotopic Ossification Management: Revitalizing Therapeutic Strategies.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Mechanisms of dexamethasone-induced bone toxicity in developing bone: a single-cell perspective.JBMR plus · 2025Article
- miR-125b differentially impacts mineralization in dexamethasone and calcium-treated human mesenchymal stem cells.Molecular therapy. Nucleic acids · 2025Article
- Forkhead box O-1 regulates the biological behavior of BMP-2-induced human bone mesenchymal stem cells through mitochondrial dynamics and autophagy.Biomolecules & biomedicine · 2025Article
- Isolation and Culture of Osteoblasts.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Identification of lactylation-related biomarkers in osteoporosis from transcriptome and single-cell data.Frontiers in endocrinology · 2025Article
- Dynamic evolution of bone marrow adipocyte in B cell acute lymphoblastic leukemia: insights from diagnosis to post-chemotherapy.Cancer biology & therapy · 2024Article
- Article
49 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dexamethasone (Dex)-induced osteoporosis has been described as the most severe side effect in long-term glucocorticoid therapy. The decreased bone mass and the increased marrow fat suggest that Dex possibly shifts the differentiation of bone marrow stromal cells (BMSCs) to favor adipocyte over osteoblast, but the underlying mechanisms are still unknown. In this paper, we established a Dex-induced osteoporotic mouse model, and found that BMSCs from Dex-treated mice are more likely to differentiate into adipocyte than those from control mice, even under the induction of bone morphogenetic protein-2 (BMP2). We also discovered both in vitro and in vivo that the expression level of adipocyte regulator CCAAT/enhancer-binding protein alpha (C/EBPalpha) is significantly upregulated in Dex-induced osteoporotic BMSCs during osteoblastogenesis by a mechanism that involves inhibited DNA hypermethylation of its promoter. Knockdown of C/EBPalpha in Dex-induced osteoporotic cells rescues their differentiation potential, suggesting that Dex shifts BMSC differentiation by inhibiting C/EBPalpha promoter methylation and upregulating its expression level. We further found that the Wnt/beta-catenin pathway is involved in Dex-induced osteoporosis and C/EBPalpha promoter methylation, and its activation by LiCl rescues the effect of Dex on C/EBPalpha promoter methylation and osteoblast/adipocyte balance. This study revealed the C/EBPalpha promoter methylation mechanism and evaluated the function of Wnt/beta-catenin pathway in Dex-induced osteoporosis, providing a useful therapeutic target for this type of osteoporosis.
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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.