ArticleStem cells international2023
Human Mesenchymal Stem Cells-Derived Exosome Mimetic Vesicles Regulation of the MAPK Pathway and ROS Levels Inhibits Glucocorticoid-Induced Apoptosis in Osteoblasts.
Article in Stem cells international, 2023. 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, 14 citations in OpenAlex.
- Enhancing osteoporosis treatment: emerging roles of engineered exosomes in bone regeneration and repair.Journal of translational medicine · 2026Review
- Engineered exosome biomedical technologies for precision diagnosis and therapy in orthopedic diseases.Frontiers in medicine · 2026Review
- CD14+ Monocytes Will Become a New Target for the Treatment of Osteoporosis: Based on Mendel Randomization, Clinical Analysis and Cell Experiment Verification.Journal of cellular and molecular medicine · 2026Article
- Mesenchymal stem cells: A new strategy for the treatment of femoral head necrosis.Regenerative therapy · 2025Review
- Immunoregulatory orchestrations in osteoarthritis and mesenchymal stromal cells for therapy.Journal of orthopaedic translation · 2025Review
- Research progress on mesenchymal stem cell‑derived exosomes in the treatment of osteoporosis induced by knee osteoarthritis (Review).International journal of molecular medicine · 2025Review
- ECHS1: pathogenic mechanisms, experimental models, and emerging therapeutic strategies.Orphanet journal of rare diseases · 2025Review
- NR2F6 promotes the malignant progression of neuroblastoma as an indicator of poor prognosis.PloS one · 2025Article
- Amniotic fluid-derived stem cells: potential factories of natural and mimetic strategies for congenital malformations.Stem cell research & therapy · 2024Article
- Advancements in diabetic foot ulcer research: Focus on mesenchymal stem cells and their exosomes.Heliyon · 2024Review
- Amniotic fluid-derived stem cells: potential factories of natural and mimetic strategies for congenital malformations.Research square · 2024Article
- Exosomal communication: a pivotal regulator of bone homeostasis and a potential therapeutic target.Frontiers in pharmacology · 2024Review
- Exploration of altered miRNA expression and function in MSC-derived extracellular vesicles in response to hydatid antigen stimulation.Frontiers in microbiology · 2024Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Long-term extensive use of glucocorticoids will lead to hormonal necrosis of the femoral head, and osteoblasts play an important role in the prevention of osteonecrosis. However, there is no complete cure for necrosis of the femoral head. Mesenchymal stem cell- (MSCs-) derived exosomes are widely used for the repair of various tissue lesions. Therefore, the aim of this study was to investigate the mechanism of dexamethasone- (DEX-) induced osteoblast apoptosis and the therapeutic effect of human umbilical cord MSC- (hucMSC-) derived exosome mimetic vesicles (EMVs) on osteoblast-induced apoptosis by DEX. Methods: The viability and apoptosis of primary MC3T3-E1 cells were determined by the Cell Counting Kit-8 (CCK-8), FITC-Annexin V/PI staining and immunoblot. The intracellular levels of reactive oxygen species (ROS) after DEX treatment were measured by 2', 7' -dichlorodihydrofluorescein diacetate (DCFH-DA) staining. In this study, hucMSC-EMVs and Results: DEX significantly induced osteoblasts MC3T3-E1 apoptosis and ROS accumulation. MAPK-signaling pathway was activated in MC3T3-E1 after DEX treatment. hucMSC-EMVs intervention significantly downregulated DEX-induced MAPK-signaling pathway activation and ROS accumulation. In addition, hucMSC-EMVs can reduce the apoptosis levels in osteoblast MC3T3-E1 cells induced by DEX. Conclusions: Our study confirmed that hucMSC-EMVs regulates MAPK-signaling pathway and ROS levels to inhibit DEX-induced osteoblast apoptosis.
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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.