Endothelial progenitor cells and vascular dysfunction in children with obstructive sleep apnea
Leila Kheirandish-Gozal1, Rakesh Bhattacharjee, Jinkwan Kim
1Section of Pediatric Sleep Medicine, Department of Pediatrics, The University of Chicago, 5721 S Maryland Avenue, MC 8000, Suite K-160, Chicago, IL 60637, USA.
Summary
Children with obstructive sleep apnea syndrome (OSAS) often have endothelial dysfunction. This dysfunction is linked to reduced endothelial progenitor cells (EPCs), indicating impaired repair mechanisms in pediatric OSAS.
Area of Science:
- Pediatric Cardiology
- Sleep Medicine
- Vascular Biology
Background:
- Obstructive sleep apnea syndrome (OSAS) in children is associated with systemic inflammation and potential endothelial dysfunction.
- However, the variability in endothelial function among children with OSAS is not fully understood.
Purpose of the Study:
- To investigate the role of endothelial progenitor cells (EPCs) in mediating endothelial function variability in pediatric OSAS.
- To explore the relationship between EPCs, stromal cell-derived factor-1 (SDF-1), and endothelial function in children with OSAS.
Main Methods:
- Assessed endothelial function using a modified hyperemic test in children with and without OSAS.
- Quantified EPCs via flow cytometry and measured SDF-1 levels by ELISA in peripheral blood samples.
- Correlated endothelial function parameters with EPC counts, SDF-1 levels, and apnea-hypopnea index (AHI).
Main Results:
- Children with OSAS exhibited delayed capillary reperfusion (Tmax), with significant variability.
- Lower EPC counts and SDF-1 levels were observed in OSAS children with the most impaired endothelial function (longest Tmax).
- Tmax was inversely correlated with EPCs, but neither parameter correlated with AHI.
Conclusions:
- Endothelial dysfunction is common in pediatric OSAS, with varying severity.
- The ability to recruit endothelial repair mechanisms, particularly EPCs, may explain the observed differences in endothelial function among children with OSAS.
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