ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024
Bmi-1 Epigenetically Orchestrates Osteogenic and Adipogenic Differentiation of Bone Marrow Mesenchymal Stem Cells to Delay Bone Aging.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. 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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15 citing papers in PubMed.
- Age-Related Lamin B1 Deficiency Activates SLC7A11-Dependent Disulfidptosis to Impair Osteogenesis via Intercepting Mitochondrial Fission.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
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- A sustained NADBioactive materials · 2026Article
- Naringenin ameliorates postmenopausal osteoporosis by inhibiting BMSC oxidative stress via the PI3K/AKT/NRF2 pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- From cell to disease: Regulatory networks and mechanisms of super‑enhancers in aging (Review).Molecular medicine reports · 2026Review
- GLP-1 regulates osteo-adipogenic fate of BMSCs via HIF-2-AKT signaling and supports trabecular bone in glucocorticoid-induced osteoporosis.Stem cell reports · 2026Article
- SERINC3 promotes osteogenic differentiation of BMSCs via IL-32/AMPK-mediated autophagy and mitochondrial energy metabolism.Stem cell research & therapy · 2026Article
- The role of the lymphatic system in musculoskeletal system health and disease: research progress and future directions.Bone research · 2026Review
- Research Hotspots and Emerging Trends in Osteoporosis Epigenetics.Genetics research · 2026Article
- Article
- The Otto Aufranc Award: DNMT3A-PPARγ Signaling Is a Key Epigenetic Mechanism of Hip Osteoarthritis Disease: A Potential Therapeutic Target.The Journal of arthroplasty · 2025Article
- Fibroblasts-specific p16Clinical and translational medicine · 2025Article
- Thymic Bmi-1 hampers γδT17 generation and its derived RORγt-IL-17A signaling to delay cardiac aging.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Effect of pyrroloquinoline quinone on skin aging in Bmi-1 KO mice and underlying mechanisms.PloS one · 2025Article
- Bmi-1 Epigenetically Orchestrates Osteogenic and Adipogenic Differentiation of Bone Marrow Mesenchymal Stem Cells to Delay Bone Aging.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
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Abstract
With the increase in the aging population, senile osteoporosis (SOP) has become a major global public health concern. Here, it is found that Prx1 and Bmi-1 co-localized in trabecular bone, bone marrow cavity, endosteum, and periosteum. Prx1-driven Bmi-1 knockout in bone-marrow mesenchymal stem cells (BMSCs) reduced bone mass and increased bone marrow adiposity by inhibiting osteoblastic bone formation, promoting osteoclastic bone resorption, downregulating the proliferation and osteogenic differentiation of BMSCs, and upregulating the adipogenic differentiation of BMSCs. However, Prx1-driven Bmi-1 overexpression showed a contrasting phenotype to Prx1-driven Bmi-1 knockout in BMSCs. Regarding mechanism, Bmi-1-RING1B bound to DNMT3A and promoted its ubiquitination and inhibited DNA methylation of Runx2 at the region from 45047012 to 45047313 bp, thus promoting the osteogenic differentiation of BMSCs. Moreover, Bmi-1-EZH2 repressed the transcription of Cebpa by promoting H3K27 trimethylation at the promoter region -1605 to -1596 bp, thus inhibiting the adipogenic differentiation of BMSCs. It is also found that Prx1-driven Bmi-1 overexpression rescued the SOP induced by Prx1-driven Bmi-1 knockout in BMSCs. Thus, Bmi-1 functioned as a hub protein in the epigenetic regulation of BMSCs differentiation to delay bone aging. The Prx1-driven Bmi-1 overexpression in BMSCs can be used as an approach for the translational therapy of SOP.
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