ArticleJournal of molecular medicine (Berlin, Germany)2017
MCP1 triggers monocyte dysfunctions during abnormal osteogenic differentiation of mesenchymal stem cells in ankylosing spondylitis.
Article in Journal of molecular medicine (Berlin, Germany), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 59 citations in OpenAlex.
- Article
- Vitamin DScientific reports · 2025Article
- Investigating the causal relationship between immune factors and ankylosing spondylitis: insights from a Mendelian Randomization study.Advances in rheumatology (London, England) · 2024Article
- Extracellular Vesicles Derived from Ligament Tissue Transport Interleukin-17A to Mediate Ligament-To-Bone Crosstalk in Ankylosing Spondylitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Sequence of Events in the Pathogenesis of Axial Spondyloarthritis: A Current Review-2023 SPARTAN Meeting Proceedings.Current rheumatology reports · 2024Review
- Osteogenic Differentiation of Human Periodontal Ligament Stromal Cells Influences Their Immunosuppressive Potential toward Allogenic CD4International journal of molecular sciences · 2023Article
- Adipokines regulate mesenchymal stem cell osteogenic differentiation.World journal of stem cells · 2023Review
- Dedifferentiated fat cells administration ameliorates abnormal expressions of fatty acids metabolism-related protein expressions and intestinal tissue damage in experimental necrotizing enterocolitis.Scientific reports · 2023Article
- Biology and therapeutic potential of mesenchymal stem cell extracellular vesicles in axial spondyloarthritis.Communications biology · 2023Review
- The m6A methyltransferase METTL16 negatively regulates MCP1 expression in mesenchymal stem cells during monocyte recruitment.JCI insight · 2023Article
- How Has Molecular Biology Enhanced Our Undertaking of axSpA and Its Management.Current rheumatology reports · 2023Review
- Evaluation of preclinical efficacy of human umbilical cord mesenchymal stem cells in ankylosing spondylitis.Frontiers in immunology · 2023Article
- LncRNA MRF drives the regulatory function on monocyte recruitment and polarization through HNRNPD-MCP1 axis in mesenchymal stem cells.Journal of biomedical science · 2022Article
- Monocyte Chemotactic Proteins Mediate the Effects of Hyperglycemia in Chondrocytes: In Vitro Studies.Life (Basel, Switzerland) · 2022Article
- Transfer of microRNA-22-3p by M2 macrophage-derived extracellular vesicles facilitates the development of ankylosing spondylitis through the PER2-mediated Wnt/β-catenin axis.Cell death discovery · 2022Article
- Osteogenic differentiation of mesenchymal stem cells promotes c-Jun-dependent secretion of interleukin 8 and mediates the migration and differentiation of CD4Stem cell research & therapy · 2022Article
- Article
- Joint together: The etiology and pathogenesis of ankylosing spondylitis.Frontiers in immunology · 2022Review
- TNF-α-mediated mNature communications · 2021Observational
- Altered Secretome of Diabetic Monocytes Could Negatively Influence Fracture Healing-An In Vitro Study.International journal of molecular sciences · 2021Article
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ankylosing spondylitis (AS) is a chronic inflammatory disease characterized by pathological osteogenesis and inflammation. However, the pathogenesis of AS and the pathological relationship between osteogenesis and inflammation in this disease remain largely unknown. Mesenchymal stem cells (MSCs) are multipotent progenitor cells capable of osteogenic differentiation and immunoregulation. Recently, we demonstrated that MSCs from AS patients (ASMSCs) have a greater potential for osteogenic differentiation than MSCs from healthy donors (HDMSCs), which therefore seems to be a component of pathological osteogenesis in AS. Previous studies have indicated that the immunoregulatory abilities of MSCs change following differentiation. However, the subsequent effects of ASMSCs during abnormal osteogenic differentiation are unclear. Here, we further demonstrated that ASMSCs secreted more monocyte chemoattractant protein 1 (MCP1) than HDMSCs during osteogenic differentiation. This enhanced MCP1 secretion augmented monocyte migration, increased classical macrophage polarization, and enhanced TNF-α secretion. Inhibiting MCP1 secretion from osteogenic differentiated ASMSCs using lentiviruses encoding short hairpin RNAs ameliorated these dysfunctions. Blocking the ERK1/2 pathway in ASMSCs with U0126 corrected the abnormal osteogenic differentiation, inhibited MCP1 overexpression, and prevented subsequent monocyte dysfunction. Finally, MCP1 expression was up-regulated during osteogenic differentiation in ASMSCs in vivo and was locally augmented in osteoblasts at ossification sites in AS patients. In summary, our study determined that MCP1 overexpression during abnormal osteogenic differentiation of ASMSCs triggers monocyte dysfunctions. We propose the novel hypothesis that pathological osteogenesis can lead to inflammation in AS. This hypothesis may contribute to reveal the precise pathological relationship between osteogenesis and inflammation in the field of osteoimmunology. KEY MESSAGE: ASMSCs secreted more MCP1 during abnormal osteogenic differentiation. MCP1 overexpression leads to monocyte dysfunctions. Pathological osteogenesis can lead to inflammation in AS.
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