Circulating extracellular vesicles from patients with acute chest syndrome disrupt adherens junctions between endothelial cells.

ABSTRACT:

Background

Small cell-derived extracellular vesicles (EVs) can affect endothelial function. We previously found that patients with sickle cell disease (SCD) have greater numbers of circulating EVs than subjects without the disease, and the EVs differentially disrupt endothelial integrity in vitro. Because endothelial disruption is a critical component of acute chest syndrome (ACS), we hypothesized that EVs isolated during ACS would induce greater endothelial damage than those isolated at baseline.

Methods

Nine pediatric subjects had plasma isolated at baseline and during ACS from which EVs were isolated. Cultured microvascular endothelial cells were treated with EVs and then studied by immunofluorescence microscopy to localize VE-cadherin and F-actin.

Results

The EVs

SUBMITTER: Lapping-Carr G 

PROVIDER: S-EPMC8261277 | biostudies-literature | 2021 Mar

REPOSITORIES: biostudies-literature