ArticleFrontiers in cell and developmental biology2025
Engineered mesenchymal stromal cells with interleukin-1beta sticky-trap attenuate osteoarthritis in knee joints.
Article in Frontiers in cell and developmental biology, 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.
- Stem Cell and Cell-Free Strategies for Osteoarthritis: Toward Durable Regenerative Therapies.Stem cells international · 2026Review
- Synovial fluid as a complex molecular pool contributing to knee osteoarthritis.Nature reviews. Rheumatology · 2025Review
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Authors and funding
9 authors.
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Abstract
Osteoarthritis (OA) is a common chronic inflammatory joint disease, in which innate immunity plays a pivotal role in pathogenesis. Anti-interleukin-1(IL-1) therapies have shown inconsistent results in clinical trials, potentially due to a mismatch in the spatial and temporal dynamics of interleukin-1beta (IL-1β) production and therapeutic interventions. To address this issue, we developed a novel IL-1β "sticky-trap" utilizing cell and gene-based technologies from our lab and evaluated its efficacy in reducing osteoarthritis progression using a murine destabilization of the medial meniscus (DMM) OA model and a compact bone-derived mesenchymal stromal cell (MSC)-based gene expression system. The extracellular domain of interleukin-1 receptor 2 (IL1R2) was employed to design the sticky IL1R2 trap (stkIL1R2). A murine compact bone-derived MSC line was engineered for gene delivery. Although stkIL1R2 was undetectable in the engineered MSC supernatants by enzyme-linked immunosorbent assay (ELISA) and Western blot, it was localized on the cell surface and extracellular matrix (ECM) and demonstrated specific binding to IL-1β using a fluorescent protein-fused binding assay. Doxycycline (Dox)-induced expression of stkIL1R2 significantly inhibited lipocalin-2 (LCN2) expression which is a biomarker of IL-1β activity. For
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