ArticleEndocrine2025
Mesenchymal stromal cells and their secretory products reduce the inflammatory crosstalk between islets and endothelial cells.
Article in Endocrine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
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Who cites it
5 citing papers in PubMed.
- Article
- The SHEDs-derived apoptotic bodies for inflammatory regulation in spinal cord repair.NPJ Regenerative medicine · 2026Article
- Diversity and Predicted Impact of miRNAs in Human MSCs-derived Extracellular Vesicles.Stem cell reviews and reports · 2026Article
- Small things matter: Lack of extraislet β cells in type 1 diabetes.Science advances · 2025Article
- Fibroblast Growth Factor 19 (FGF-19) Expression in Glycoresistant Human Umbilical Cord Mesenchymal Stem Cells (ghUC-MSCs) and Its Regulatory Effect on Glucose Metabolism in Insulin-Resistant Hepatocytes.Dose-response : a publication of International Hormesis SocietyArticle
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
purposePreculturing isolated islets with Mesenchymal Stromal Cells (MSCs) improves their functional survival in vitro and subsequent transplantation outcomes in vivo. The MSC secretory product Annexin A1 (ANXA1) is a key modulator of MSC-mediated improvements in islet function. The current study aims to determine the influence of MSCs and defined MSC secretory products, including ANXA1, on the inflammatory crosstalk between isolated islets and Endothelial Cells (ECs), using in vitro models of the clinically-preferred intraportal islet transplantation niche.
methodsIslets were cultured alone, with MSCs, or with MSC secretory products and exposed to pro-inflammatory cytokines. Islet gene expression of C-C Motif Chemokine Ligand 2 (CCL2), C-X-C Motif Chemokine Ligand (CXCL)-10 (CXCL10) and CXCL1 were assessed by RT-qPCR. EC activation was induced with 100 U/ml TNF for 24 h. Islet-EC co-cultures were used to determine the influence of MSCs, or MSC secretory products on the inflammatory crosstalk between isolated islets and ECs. VCAM-1 and ICAM-1 expression were assessed at the mRNA and protein level in ECs, using RT-qPCR and immunofluorescence.
resultsMSCs reduce pro-inflammatory cytokine-induced islet CCL2, CXCL10, and CXCL1 gene expression, which is partially mimicked by ANXA1. MSCs and ANXA1 have a similar capacity to reduce TNF-induced EC activation. Isolated islets exacerbate TNF-induced EC activation. Preculturing islets with MSCs reduces islet-exacerbated EC activation. ANXA1 reduces islet-exacerbated EC activation, when present during the islet preculture and islet-EC co-culture period.
conclusionMSC-derived secretory factors, including ANXA1, may be used in islet transplantation protocols to target donor islet and host EC inflammation at the intraportal niche.
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