Endocrinology · 4 h ago
Umbilical cord stem cell vesicles protect islet grafts in diabetic mice
In a preclinical study, extracellular vesicles from human umbilical cord mesenchymal stem cells improved graft function and reduced beta-cell apoptosis in diabetic mice. Experiments linked the effects to vesicle-delivered miR-182-5p and regulation of endoplasmic reticulum–mitochondrial calcium balance.
- EV co-transplantation improved glycaemic measures in diabetic mice.
- Grafts had fewer apoptotic beta cells.
- miR-182-5p depletion abolished reported protection.
- Human efficacy and safety remain unestablished.
Islet transplantation can be limited by early graft injury and beta-cell loss. Researchers tested extracellular vesicles from human umbilical cord mesenchymal stem cells (hucMSC-EVs) in a syngeneic islet-transplant model using streptozotocin-induced diabetic mice. They also studied primary islets and beta cells exposed to endoplasmic reticulum stress in laboratory experiments. The abstract does not report the number of animals or islets used per group.
Co-transplantation of hucMSC-EVs with 250 islet equivalents improved glycaemic control and glucose tolerance compared with grafts without EVs (both p<0.01). Grafts receiving EVs had fewer apoptotic beta cells, while laboratory assays found preserved insulin expression and glucose-stimulated insulin secretion. Mechanistic experiments implicated EV-enriched miR-182-5p, which targeted XBP1 and was associated with restored calcium homeostasis and mitochondrial function. Depleting miR-182-5p removed the reported protective effects in mice.
These findings suggest a potential cell-free approach to protecting islet grafts, but the evidence is preclinical. The study does not establish safety, efficacy, or a role for hucMSC-EVs in human transplantation; clinical benefit cannot be inferred from these mouse and cell experiments.
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Diabetologia: Extracellular vesicles from human umbilical cord mesenchymal stem cells protect grafted islets against endoplasmic reticulum stress-induced mitochondrial dysfunction via modulating XBP1-based calcium homeostasis ↗This is an automated AI-condensed summary that has not yet been reviewed by an editor. Always consult the full item at the original source.
