Thread by @CVR_TomaszGuzik

Endothelial-derived microvesicles play a pathogenic role in vascular #inflammation, causing #endothelial barrier dysfunction by impairing adherens junctions and activating #neutrophils

More here: bit.ly/3g1FpH7
#Cardiotwitter #CardiovascularResearch

#Tweetorial below!

#Microvesicles (MV) are formed from the outward blebbing of the plasma membrane and carry a diverse cargo that regulate multiple processes.

During #inflammation these are produced by activated endothelial cells and released into the #circulation. TEM image of plasma MVs: (2/8)

In this study the authors investigated whether endothelial-derived MVs (EC-MVs) contribute to #vascular dysfunction during inflammation.

The authors used an animal model of #sepsis (CLP) and found that this increased EC-MV production (3/8)

The authors next stimulated cultured #endothelial cells with different #proinflammatory agents known to increase in the circulation during sepsis. They found that these produced a diverse range of EC-MVs and cargo (4/8)

EC-MVs were topically applied to #endothelial cells causing:

-#Junction and #cytoskeleton protein phosphorylation
-Contractile fibre reorganization
-#Adherens junction dissociation
-Increased endothelial #permeability to albumin
(5/8)

Barrier #dysfunction caused by EC-MVs were coupled with #protein #phosphorylation mediated by MV cargos containing c-Src. However, MVs produced from c-Src deficient cells did not exert barrier-disrupting effects (6/8)

In addition, EC-MVs contributed indirectly to #vascular #injury by increasing the surface expression of adhesion molecules on endothelial cells and activating #neutrophils (7/8)

In conclusion, this study shows #endothelial production of MVs contribute to vascular dysfunction during #inflammation by carrying Src-bearing cargo that interact with endothelial cells. EC-MVs can also stimulate neutrophil-endothelium adhesion (8/8)