ArticleStem cell research & therapy2025
Human urine-derived stem cells alleviate psoriasis by suppressing JAK2/STAT3 pathway-mediated macrophage polarization.
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 3 papers.
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Who cites it
3 citing papers in PubMed.
- Urine-Derived Stem Cells: Challenges in Isolation, Biological Identity, and Therapeutic Potential in CKD-Associated Fibrosis.International journal of molecular sciences · 2026Review
- Rewired DDR-TGF-β-β-catenin-PD-L1 axis accelerates progression and shapes therapy in human papillomavirus-driven cancer.Frontiers in immunology · 2026Review
- Targeting macrophage polarization: mechanisms and potential of mesenchymal stromal/stem cells therapy in acne treatment- a narrative review.Frontiers in immunology · 2026Review
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Authors and funding
9 authors.
Funding
Abstract
backgroundPsoriasis is a chronic skin disease featured with aberrant keratinocyte proliferation, inflammatory cell infiltration, and immune dysregulated. Although the imbalance of M1/M2 macrophage polarization is implicated in its pathogenesis, the underlying mechanisms remain unclear. Mesenchymal stem cells exhibited potent immunomodulatory properties, representing a promising therapeutic approach for psoriasis. This study aimed to explore the role and the underlying mechanism of human urine-derived stem cells (hUSCs) in mouse psoriatic models.
methodshUSCs were isolated from urine of heath volunteer and cultured in serum-free medium, and characterized by multiple approaches such as morphological analysis, biological markers examination, differentiation potentials and tumorigenicity assay. Histological analysis, immunofluorescence staining, ELISA, flow cytometry, antibody array, western blot and qRT-PCR analysis were used to assess the therapeutic effects and the underlying mechanism of hUSCs in imiquimod (IMQ)-induced mouse psoriasis models and multiple cell models.
resultshUSCs had the potential for self-renewal and multipotent differentiation with low immunogenicity and lacking tumorigenicity both in vitro and in vivo. Our results showed that hUSCs significantly alleviated IMQ-induced psoriasis via their paracrine, evidenced by improving morphologies, inhibiting the infiltration of macrophages, reducing the releases of the pro-inflammatory cytokines. Mechanistically, we revealed that the protective effects of hUSCs on psoriasis were involved in suppressing M1 and promoting M2 macrophage polarization, and inhibiting NETs formation through inhibiting JAK2/STAT3 pathway. Finally, we further demonstrated that hUSCs-derived TGF-β1 selectively inhibited the JAK2/STAT3 pathway-mediated the polarization of M1 and M2 macrophages to alleviate psoriasis in mouse and cellular models.
conclusionsOur data demonstrated that hUSCs remarkably ameliorated psoriasis by suppressing M1 and promoting M2 macrophage polarization through they-derived TGF-β1 inhibiting the JAK2/STAT3 pathway. Our results have revealed the molecular mechanism of hUSCs in treating psoriasis, highlighting a safe and effective cellular treatment method for psoriasis.
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