AI Article Synopsis

  • Mesenchymal stem cells (MSCs) show potential in treating type 1 diabetes mellitus (T1DM) by possibly affecting T cell behavior, but the exact mechanisms are not fully understood.
  • The study identified that miR-25, found in MSCs' exosomes, is linked to cell migration and can decrease CXCR3 expression in activated T cells, reducing their movement towards the pancreas.
  • In experiments with T1DM mouse models, MSC treatment raised miR-25 levels and reduced T cell numbers in the pancreas, indicating that miR-25 may help prevent T cell infiltration in T1DM.

Article Abstract

Mesenchymal stem cells (MSCs) have demonstrated promising therapeutic potential in the treatment of type 1 diabetes mellitus (T1DM); however, the underlying mechanism remains unclear. The primary pathological mechanism of T1DM involves activated T cells infiltrating the pancreas, leading to islet inflammation and the destruction of β-cells. However, the question of whether exosomes derived from MSCs can suppress the migration of T cells to the pancreas in the context of T1DM remains unresolved. In this study, we observed that miR-25 was highly expressed in MSCs exosomes and associated with signaling pathways related to cell migration. In vitro assay, we synthesized a miR-25 mimic and transiently transfected it into activated T cells, which revealed that miR-25 can effectively reduce the expression of CXCR3. Additionally, according to the in vivo T1DM mouse model, we found that there was a significant increase in miR-25 levels in T1DM mice treated with MSCs and the number of T cells decreased. Overall, our findings suggest that MSCs exosomes containing miR-25 can impede the infiltration of activated T cells into the pancreas in T1DM by repressing CXCR3 expression in these cells.

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Source
http://dx.doi.org/10.1016/j.gene.2024.149098DOI Listing

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