ArticleIn vitro cellular & developmental biology. Animal2025
Therapeutic potential of miR-10a overexpressing mesenchymal stem cell-derived extracellular vesicles in modulating inflammation in collagen-induced arthritis.
Article in In vitro cellular & developmental biology. Animal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Ribosomal proteins, miRNAs, and extracellular vesicles in myelodysplastic syndromes: molecular regulation and biomarker potential.Frontiers in oncology · 2026Review
- Extracellular vesicles in rheumatoid arthritis: emerging roles in progression, diagnosis, and therapeutic development.Frontiers in immunology · 2026Review
- Immunocyte-derived extracellular vesicles in osteoimmunology: mechanisms, disease contexts, and translational prospects.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Rheumatoid arthritis (RA) is a chronic autoimmune condition that leads to joint damage. Mesenchymal stem cells (MSCs) are being recognized as a promising treatment option because of their capacity to modulate immune responses. Their therapeutic effects are mediated by released extracellular vesicles (EVs) which contain microRNAs known to influence inflammatory processes. This research focused on the impact of bone marrow MSC (BM-MSC)-derived EVs overexpressing miR-10a on cytokine production in a mouse model of collagen-induced arthritis (CIA). miR-10a was overexpressed in MSCs derived from bone marrow using Transfectamin. EVs were then isolated from the culture media of both miR-control and miR-10a-modified MSCs. Immunizing mice established the CIA model with type II collagen, after which they received either miR-control or miR-10a-enriched MSC-EVs. The severity of arthritis was evaluated through joint swelling measurements, and the concentrations of pro-inflammatory cytokines (such as interleukin (IL)-17a, interferon (IFN)-γ, and tumor necrosis factor (TNF)-α) alongside anti-inflammatory cytokines (including transforming growth factor (TGF)-β, IL-10, and IL-4) in the joints and serum were assessed using real-time PCR and enzyme-linked immunosorbent assay (ELISA), respectively. Our results indicated that treatment with miR-10a MSC-EVs led to a notable decrease in arthritis severity and joint damage in CIA mice. Furthermore, these EVs were found to lower levels of pro-inflammatory cytokines while enhancing anti-inflammatory cytokines compared to those treated with miR-control MSC-EVs. This study highlights how enhancing miR-10a expression can improve the therapeutic efficacy of MSC-EVs by altering the cytokine environment in CIA models.
Indexed as
Identifiers
40751028What OpenQuestion holds
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.