ArticleFrontiers in cell and developmental biology2025
Menstrual blood-derived mesenchymal stromal cell secretome modulates macrophage polarization in a preconditioning-dependent manner.
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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2 citing papers in PubMed.
- A pro-inflammatory metastasis-associated macrophage subset induces tumor-promoting mesothelial cell conversion in ovarian cancer via IL-1α secretion.Cell death & disease · 2026Article
- Single-cell and spatial transcriptomics reveal Thbs1-CD36 crosstalk between Kupffer and hepatic stellate cells following mesenchymal stem cell-derived small extracellular vesicles transplantation, alleviating liver fibrosis.Journal of nanobiotechnology · 2026Article
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13 authors.
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Abstract
Background: The effects of menstrual blood-derived mesenchymal stromal cell secretome (S-MenSC) on macrophage polarization remain unclear. This study studied the impact of secretomes from basal MenSCs (S-bMenSCs) and those preconditioned with IFNγ and TNFα (S-pMenSCs) on human monocytes and macrophages Methods: S-MenSCs were used to assess their effects on three stages of monocyte-derived cell maturation: i. monocyte differentiation; ii. polarization of monocyte-derived macrophages (MDMs) toward M1-like or M2-like phenotypes; and iii. reprogramming of pre-polarized M1 or M2 macrophages. Surface markers were analyzed by flow cytometry and cytokine gene expression by RT-qPCR. In addition, a proteomic profiling was performed to identify proteins involved in the observed effects. Results: Our results confirmed the capacity of S-MenSCs of modulating innate immune response and in particular macrophage polarization. More concretely, the Conclusion: These findings extend the knowledge on the immunomodulatory capacity of the S-MenSC, supporting that MenSCs, particularly when preconditioned, may play a significant role in regulating macrophage polarization, and, thus, modulating the inflammatory response.
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