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Exosomes contribute to endothelial integrity and acute chest syndrome risk: Preliminary findings
Gabrielle Lapping-Carr1, Abdelnaby Khalyfa2, Stephanie Rangel3
1Sections of Pediatric Hematology-Oncology,, Department of Pediatrics, Comer Children's Hospital, The University of Chicago, Chicago, Illinois.
Insights
Exosomes from children with Sickle Cell Disease (SCD) who experienced Acute Chest Syndrome (ACS) impair blood vessel function. These exosomes may contribute to ACS and serve as potential biomarkers for risk in SCD patients.
Area of Science:
- Vascular Biology
- Hematology
- Cell Biology
Background:
- Acute Chest Syndrome (ACS) is a major cause of mortality in children with Sickle Cell Disease (SCD).
- Endothelial dysfunction and microvascular integrity disruption are key to ACS.
- The role of circulating exosomes in ACS pathophysiology is not well understood.
Purpose of the Study:
- To investigate the hypothesis that exosomes from patients with SCD induce endothelial dysfunction, particularly in those who have experienced ACS.
Main Methods:
- A cross-sectional study involving 33 SCD outpatients and control patients.
- Exosomes were isolated from platelet-free plasma.
- Endothelial cell resistance was measured using Electric Cell-substrate Impedance Sensing (ECIS) after treatment with patient-derived exosomes.
Main Results:
- Exosome counts were significantly higher in SCD patients compared to controls.
- Exosomes from ACS(+) SCD patients reduced endothelial cell resistance compared to ACS(-) patients.
- ACS(+)-derived exosomes failed to increase eNOS mRNA expression, unlike exosomes from ACS(-) patients.
Conclusions:
- Circulating exosomes in SCD patients exhibit differential effects on endothelial cells.
- These exosome-mediated effects may contribute to ACS development.
- Exosomes in SCD could serve as potential biomarkers for ACS risk.
Background:
Acute Chest Syndrome (ACS) is one of the leading causes of death among children with Sickle Cell Disease (SCD). Disruption of microvascular integrity is critical to the pathophysiology of ACS, but the factors governing its phenotypic variability are incompletely understood. Because circulating exosomes have been implicated in vascular dysfunction in various diseases, we hypothesized that exosomes induce endothelial dysfunction in patients who experience ACS.
Procedure:
Cross-sectional cohort study including 33 outpatients with SCD (without new health-related complaints or recent transfusions) and a cohort of control patients. Exosomes were isolated from platelet-free plasma.
Results:
ImageStream showed that exosome counts were greatly increased in patients with SCD compared with controls, but there were few differences in the concentrations of exosomes between patients who had experienced ACS (ACS(+)) and those who had not (ACS(-)). Exosomes were added to human microvascular endothelial cells, and the exosomal effects on monolayer integrity was determined using Electric Cell-substrate Impedance Sensing (ECIS). Exosomes from SCD patients without ACS differed minimally from control patients; however, exosomes from ACS(+) decreased endothelial cell resistance compared to ACS(-), (Relative resistance: ACS(+): 0.981 ± 0.055 vs ACS(-): 1.124 ± 0.042; P = 0.006). Treatment of endothelial cultures with exosomes from ACS(-) patients increased endothelial Nitric Oxide Synthase (eNOS) mRNA expression, while ACS(+)-derived exosomes were not able to increase eNOS expression above that of controls.
Conclusions:
These findings demonstrate that patients with SCD have circulating exosomes that produce differential effects that may contribute to the pathophysiology of ACS and may serve as risk-related biomarkers.
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