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Circulating small extracellular vesicles mediate vascular hyperpermeability in diabetes.

Dakota Gustafson1,2, Peter V DiStefano1, Xue Fan Wang3

  • 1Toronto General Hospital Research Institute, University Health Network, Toronto, ON, Canada.

Diabetologia
|March 15, 2024
PubMed
Summary

Circulating small extracellular vesicles (sEVs) from diabetic individuals increase in number and size, disrupting the vascular barrier. These diabetic sEVs activate MEK/ROCK pathways, contributing to vascular dysfunction and cognitive decline in type 2 diabetes.

Keywords:
CerebrovasculatureCognitive impairmentDiabetesEndothelial dysfunctionExtracellular vesiclesPermeabilityType 2 DiabetesVascular biologyVascular hyperpermeabilityVasculature

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Area of Science:

  • Vascular biology
  • Diabetes complications
  • Extracellular vesicles

Background:

  • Type 2 diabetes mellitus is linked to vascular hyperpermeability and cognitive impairment.
  • Cerebrovascular endothelial dysfunction is a key feature of diabetic complications.

Purpose of the Study:

  • To test if circulating small extracellular vesicles (sEVs) change in type 2 diabetes to disrupt the vascular barrier.
  • To investigate the role of sEVs in diabetic cerebrovascular dysfunction and cognitive decline.

Main Methods:

  • Isolated sEVs from diabetic and non-diabetic mice and humans.
  • Assessed sEVs' ability to disrupt endothelial cell barriers.
  • Analyzed sEV contents and effects on recipient cells using proteomics and pathway inhibitors.

Main Results:

  • Diabetic mice showed cerebrovascular hyperpermeability.
  • sEVs from diabetic mice and humans increased in quantity and size.
  • Diabetic sEVs disrupted endothelial cell barriers by modulating MEK/ROCK pathways and cell-cell junctions.

Conclusions:

  • Diabetes increases circulating sEV concentration and size.
  • Diabetic sEVs induce vascular leak via MEK/ROCK pathway activation.
  • sEVs may play a role in diabetic cerebrovascular dysfunction and cognitive decline.