ArticleCytotechnology2025
The study on bone marrow mesenchymal stem cell-derived extracellular matrix promoting the repair of damaged chondrocytes by regulating the Notch1/RBPJ pathway.
Article in Cytotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Multi-omics analysis reveals RBPJ-mediated regulation of EGF/ACTN2/MYPN/COL21A1 in fibroblast during oviduct functional remodeling of duck.Poultry science · 2026Article
- Regulation of melanin synthesis in goat hair follicles by melatonin through the Wnt/β-catenin pathway.Molecular genetics and genomics : MGG · 2025Article
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Authors and funding
7 authors.
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Abstract
Cartilage and joint damage can lead to cartilage degeneration. Bone marrow mesenchymal stem cells (BMSCs) have the potential to address cartilage damage. Hence, this study probed the mechanism of BMSC-extracellular matrix (BMSC-ECM) in promoting damaged chondrocyte repair by regulating the Notch1/RBPJ pathway. Human immortalized chondrocytes were cultured in vitro and treated with Notch1 small interfering (si)RNA, pCDNA3.1-Notch1, RBPJ siRNA and their negative controls (NCs). Damaged chondrocytes were constructed. Damaged chondrocyte-BMSC co-culture system was established and treated with lentiviral vector carrying short hairpin-Notch1 and its NC. Cell viability and apoptosis were assessed by CCK-8 and flow cytometry assays. Levels of glycosaminoglycan (GAG), Notch1 and RBPJ mRNA, and Notch1, RBPJ, Col2α1, mmp3, Hes1 and Hey1 were determined by a kit, RT-qPCR and Western blot. NICD nuclear translocation was detected by immunofluorescence. Damaged chondrocytes exhibited down-regulated Notch1 expression, reduced cell viability, and enhanced apoptosis. Further Notch1 knockdown aggravated chondrocyte damage, whereas its overexpression enhanced chondrocyte viability and decreased apoptosis. NICD translocated into the nucleus and bound to RBPJ to activate the Notch1 pathway. RBPJ silencing partly annulled Notch1-regulated damaged chondrocyte apoptosis. BMSC-damaged chondrocyte co-culture up-regulated Notch1, RBPJ, Col2α1, mmp3, Hes1, Hey1 and GAG levels, enhanced cell viability, and reduced apoptosis in chondrocytes, which were partly negated by Notch1 suppression, indicating that BMSC-ECM facilitated damaged chondrocyte repair by activating the Notch1/RBPJ pathway. BMSC-ECM promoted the repair of damaged chondrocytes by promoting NICD translocation into the nucleus and binding to RBPJ to activate the Notch1 pathway. Supplementary Information: The online version contains supplementary material available at 10.1007/s10616-024-00702-6.
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