Circulating P-Selectin Glycoprotein Ligand 1 and P-Selectin Levels in Obstructive Sleep Apnea Patients

Purpose Obstructive sleep apnea (OSA) is characterized by chronic intermittent hypoxia which induces inflammation in blood vessels leading to the development of cardiovascular comorbidities. Several studies implicated the role of P-selectin in vascular inflammation of OSA. P-selectin glycoprotein li...

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Bibliographic Details
Published in:Lung 2020-02, Vol.198 (1), p.173-179
Main Authors: Horváth, P., Lázár, Z., Gálffy, G., Puskás, R., Kunos, L., Losonczy, Gy, Mészáros, M., Tárnoki, Á. D., Tárnoki, D. L., Bikov, A.
Format: Article
Language:English
Subjects:
Diagnosis
Glycoproteins
Health aspects
Medicine
Medicine & Public Health
Obesity
Physiological aspects
Pneumology/Respiratory System
Sleep
Sleep apnea syndromes
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Summary:Purpose Obstructive sleep apnea (OSA) is characterized by chronic intermittent hypoxia which induces inflammation in blood vessels leading to the development of cardiovascular comorbidities. Several studies implicated the role of P-selectin in vascular inflammation of OSA. P-selectin glycoprotein ligand 1 (PSGL-1) is the main activator for P-selectin and is involved in immune cell trafficking. However, PSGL-1 has not been analyzed in OSA. The aim of the study was to investigate plasma PSGL-1 and P-selectin levels to have a deeper understanding on their interaction in obstructive sleep apnea. Methods Fifty-one untreated patients with OSA and 42 non-OSA controls were recruited. Plasma PSGL-1 levels were determined in evening and morning samples, P-selectin levels were analyzed in morning samples using commercially available ELISA kits. Polysomnography was performed in all participants. OSA was defined by an apnea–hypopnea index ≥ 5/h. Results PSGL-1 levels did not differ between controls and OSA patients either in the evening or in the morning. Although, there was no difference between controls (16.9/6.8–40.8 ng/ml) and patients with OSA (19.6/8.4–56.8, p  = 0.24), patients with severe OSA had increased plasma P-selectin levels (25.6/8.4–56.8 ng/ml) compared to mild OSA patients (14.1/8.5–35.3 ng/ml, p  = 0.006) and controls ( p  = 0.03). Conclusions P-selectin expression relates to disease severity suggesting a pathophysiological role in endothelial cell activation. PSGL-1 levels are unaltered in OSA, suggesting an alternative activation pathway for P-selectin in OSA.
ISSN:0341-2040
1432-1750
DOI:10.1007/s00408-019-00299-0