ArticleStem cell research & therapy2025
MSC administration resolves experimental acute gout increasing specialized pro-resolving mediators synthesis through a super-induction of prostaglandin E
Article in Stem cell research & therapy, 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.
- Mesenchymal stromal/stem cells in tumour initiation, progression and therapy.Nature reviews. Cancer · 2026Review
- Impaired Macrophage Efferocytosis: Shared Mechanisms and Therapeutic Implications in Immune-Mediated Inflammatory Diseases.Journal of inflammation research · 2026Review
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Authors and funding
7 authors.
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Abstract
backgroundThe resolution of inflammation is an active process triggered in the acute phase of inflammation and mainly directed by specialized pro-resolving mediators (SPMs). Modulating the inflammatory response in favor of resolution is a therapeutic strategy of enormous interest and value. Previous studies have shown that human adipose mesenchymal stem cells (MSCs) possess the ability to shorten the acute inflammatory response by hinting an early cyclooxygenase (COX)-2 induction. We studied the potential of MSC to accelerate the resolution of inflammation through the direct promotion of the local synthesis of SPMs, and the role of prostaglandin (PG) E
methodsGouty arthritis was induced in male New Zealand rabbits via intra-articular injection of monosodium urate (MSU) crystals. Human adipose-derived MSCs were administered systemically in a single dose. Synovial membrane levels of SPMs were measured by liquid chromatography-tandem mass spectrometry, PGE
resultsMSC treatment enhanced the local release of a broad range of SPM precursors and active mediators in the synovial membrane of rabbits with gouty arthritis. This release occurred simultaneously with an early increase in PGE₂ levels, and an upregulation of COX-2 and the PGE
conclusionsMSCs exerted a pro-resolving effect on the synovial membrane in gouty arthritis. This therapeutic action may be driven by an early superinduction of local PGE₂ synthesis and the promotion of a pro-resolving and anti-inflammatory M2 macrophage phenotype via COX-2 signaling and involving FPR2.
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