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- W3162692190 abstract "Abstract Progressive destruction of pancreatic islet β-cells by immune cells is a primary feature of type 1 diabetes (T1D) and therapies that can restore the functional β-cell mass are needed to alleviate disease progression. Here, we report the use of mesenchymal stromal/stem cells (MSCs) for the production and delivery of Gastrin, a peptide-hormone which is produced by intestinal cells and fetal islets and can increase β-Cell mass, to promote protection from T1D. A single injection of syngeneic MSCs that were engineered to express Gastrin (Gastrin-MSCs) caused a significant delay in hyperglycemia in non-obese diabetic (NOD) mice compared to engineered control-MSCs. Similar treatment of early-hyperglycemic mice caused the restoration of euglycemia for a considerable duration, and these therapeutic effects were associated with protection of, and/or higher frequencies of, insulin producing islets and less severe insulitis. While the overall immune cell phenotype was not affected profoundly upon treatment using Gastrin-MSCs or upon in vitro culture, pancreatic lymph node cells from Gastrin-MSC treated mice, upon ex vivo challenge with self-antigen, showed a Th2 and Th17 bias, and diminished the diabetogenic property in NOD- Rag1 deficient mice suggesting a disease protective immune modulation under Gastrin-MSC treatment associated protection from hyperglycemia. Overall, this study shows the potential of production and delivery of Gastrin in vivo, by MSCs, in protecting insulin producing β-cells and ameliorating the disease progression in T1D." @default.
- W3162692190 created "2021-05-24" @default.
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- W3162692190 date "2021-05-15" @default.
- W3162692190 modified "2023-10-17" @default.
- W3162692190 title "Gastrin producing syngeneic mesenchymal stem cells protect non-obese diabetic mice from type 1 diabetes" @default.
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- W3162692190 doi "https://doi.org/10.1101/2021.05.13.444059" @default.
- W3162692190 hasPublicationYear "2021" @default.
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