Circulating P-Selectin Glycoprotein Ligand 1 and P-Selectin Levels in Obstructive Sleep Apnea Patients.
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ABSTRACT:
SUBMITTER: Horvath P
PROVIDER: S-EPMC7012996 | biostudies-literature | 2020 Feb
REPOSITORIES: biostudies-literature
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Project description:Cardiac arrhythmias and sudden cardiac death are more frequent in patients with obstructive sleep apnea (OSA). OSA is associated with QT prolongation, and QT prolongation is an independent risk factor for sudden cardiac death. Because QT prolongation can be mediated by potassium channel loss of function, we tested whether OSA or continuous positive airway pressure therapy altered mRNA expression of circulating white blood cell potassium channels.In total, 28 patients with OSA newly diagnosed by polysomnogram and 6 participants without OSA were enrolled. Potassium channel levels in white blood cells at baseline and at a 4-week follow-up visit were compared. There was a significant inverse correlation between the severity of the OSA stratified by apnea-hypopnea index and mRNA expression of the main potassium channels assessed: KCNQ1 (r=-0.486, P=0.007), KCNH2 (r=-0.437, P=0.016), KCNE1 (r=-0.567, P=0.001), KCNJ2 (r=-0.442, P=0.015), and KCNA5 (r=-0.468, P=0.009). In addition, KCNQ1, KCNH2, and KCNE1 inversely correlated with the oxygen desaturation index 4. After 4 weeks of continuous positive airway pressure therapy, circulating KCNQ1 and KCNJ2 were increased 1.4±0.4-fold (P=0.040) and 2.1±1.4-fold (P=0.046) in the moderate OSA group. Compared with patients with mild or moderate OSA, patients with severe OSA had a persistently higher apnea-hypopnea index (mild 2.0±1.8, moderate 1.0±0.9, severe 5.8±5.6; P=0.015), perhaps explaining why the potassium channel changes were not seen in the severe OSA group.The mRNA expression of most potassium channels inversely correlates with the severity of OSA and hypoxemia. Continuous positive airway pressure therapy improves circulating KCNQ1 and KCNJ2 in patients with moderate OSA.
| S-EPMC5015289 | biostudies-literature
Project description:Rationale: Obstructive sleep apnea (OSA) has been associated with metabolic dysregulation and systemic inflammation. This may be due to pathophysiologic effects of OSA on visceral adipose tissue. We sought to assess the transcriptional consequences of OSA on adipocytes by utilizing pathway-focused analyses. Methods: Patients scheduled to undergo ventral hernia repair surgery were recruited to wear a portable home sleep monitor for two nights prior to surgery. Visceral fat biopsies were obtained intra-operatively. RNA was extracted and whole-genome expression profiling was performed. Gene Set Enrichment Analysis (GSEA) was used to identify curated gene sets that were differentially enriched in OSA subjects. Network analysis was applied to a select set of highly enriched pathways. Results: 10 patients with OSA and 8 control subjects were recruited. There were no differences in age, gender, body mass index between the two groups, but the OSA subjects had a significantly higher respiratory disturbance index (19.2 vs. 0.6, P-value 0.05) and worse hypoxemia (minimum oxygen saturation 79.7% vs. 87.8%, P-value < 0.001). GSEA identified a number of gene sets up-regulated in adipose tissue of OSA patients including the pro-inflammatory NF-M-NM-:B pathway and the proteolytic ubiquitin/proteasome module. A critical metabolic pathway, the peroxisome proliferator-activated receptor (PPAR), was down-regulated in subjects with OSA. Network analysis linked members of these modules together and identified regulatory hubs. Conclusions: OSA is associated with alterations in visceral fat gene expression. Pathway-based network analysis highlighted perturbations in several key pathways whose coordinated interactions may contribute to the metabolic dysregulation observed in this complex disorder. Total RNA from visceral fat of 18 subjects (10 OSA, 8 Control) was hybridized to 18 Affymetrix Genechip Human Gene 1.0 ST microarrays.
2012-09-01 | E-GEOD-38792 | biostudies-arrayexpress
Project description:Rationale: Obstructive sleep apnea (OSA) has been associated with metabolic dysregulation and systemic inflammation. This may be due to pathophysiologic effects of OSA on visceral adipose tissue. We sought to assess the transcriptional consequences of OSA on adipocytes by utilizing pathway-focused analyses. Methods: Patients scheduled to undergo ventral hernia repair surgery were recruited to wear a portable home sleep monitor for two nights prior to surgery. Visceral fat biopsies were obtained intra-operatively. RNA was extracted and whole-genome expression profiling was performed. Gene Set Enrichment Analysis (GSEA) was used to identify curated gene sets that were differentially enriched in OSA subjects. Network analysis was applied to a select set of highly enriched pathways. Results: 10 patients with OSA and 8 control subjects were recruited. There were no differences in age, gender, body mass index between the two groups, but the OSA subjects had a significantly higher respiratory disturbance index (19.2 vs. 0.6, P-value 0.05) and worse hypoxemia (minimum oxygen saturation 79.7% vs. 87.8%, P-value < 0.001). GSEA identified a number of gene sets up-regulated in adipose tissue of OSA patients including the pro-inflammatory NF-κB pathway and the proteolytic ubiquitin/proteasome module. A critical metabolic pathway, the peroxisome proliferator-activated receptor (PPAR), was down-regulated in subjects with OSA. Network analysis linked members of these modules together and identified regulatory hubs. Conclusions: OSA is associated with alterations in visceral fat gene expression. Pathway-based network analysis highlighted perturbations in several key pathways whose coordinated interactions may contribute to the metabolic dysregulation observed in this complex disorder.
2012-09-01 | GSE38792 | GEO
Project description:BackgroundObstructive sleep apnea (OSA) patients are at increased risk of cardiovascular disease (CVD). Cell adhesion molecules (CAM) are increased in OSA and CAM are also implicated in the development of CVD.Research questionDo CAM (ICAM-1, VCAM-1 and E-selectin) have prognostic value in identifying risk of cardiovascular events in OSA?Study design and methodsPatients with suspected OSA referred for a polysomnogram provided a fasting blood sample. Plasma levels of ICAM-1, VCAM-1 and E-selectin were determined by multiplex Luminex Assay (Milliporesigma ON, Canada). Cardiovascular events were determined by deterministic linkage to provincial health databases.Results418 patients were included in the analysis. Mostly male (68.2%), mean age of 50.7 yrs, median AHI 16.5 events/hour, and mean BMI of 31.7 kg/m2. 36 cardiovascular events occurred in 8-yrs of follow up. Higher levels of ICAM-1 were associated with developing CVD (HR = 3.65 95% CI 1.40-9.53, 2nd and 3rd tertiles vs. 1st tertile), including in patients with OSA (HR = 3.1 95% CI 1.16-8.25). E-selectin was significantly associated with cardiovascular events in patients with moderate to severe OSA (HR = 3.31 95% CI 0.94-11.72, 2nd and 3rd tertiles vs. 1st tertile) but not in patients without moderate to severe OSA (HR = 0.67 95% CI 0.19-2.38), p-value for interaction = 0.07.InterpretationIn a suspected OSA cohort, patients with higher levels of ICAM-1 (>816 ng/ml) were significantly more likely to experience a cardiovascular event within 8 years after PSG. In moderate to severe OSA patients, a higher E-selectin (>36.4 ng/ml) was significantly associated with cardiovascular events.
| S-EPMC8323915 | biostudies-literature
Project description:BackgroundEndothelial dysfunction is one of the most important early indicators of atherosclerosis in obstructive sleep apnea (OSA) patients. Endothelial cell specific molecules-1 (ESM-1), which is a novel endothelial dysfunction marker that may be linked to cardiovascular disease. We investigated to assess whether circulating ESM-1 levels are correlated with the presence of coronary artery disease (CAD) in patients with OSA.MethodsWe performed a cross-sectional study in 228 Chinese OSA subjects, including 185 patients with OSA and 43 controls. The Gensini stenosis scoring system was used to assess the severity of CAD. Circulating ESM-1 levels were measured by Human Magnetic Luminex Screening Assay. The associations between circulating ESM-1 levels and CAD were determined by multivariate logistic regression analysis. The association between ESM-1 levels and Gensini scores was determined by multivariate linear regression analysis.ResultsCAD patients had significantly higher circulating ESM-1 levels compared with non-CAD patients (1279.01[918.52-1770.71] pg/ml vs 585.46[423.61-812.56] pg/ml, P < 0.001). After adjusting for confounding factors, we found that circulating ESM-1 levels were an independent risk factor for CAD (OR = 1.633/100 pg ESM-1, 95%CI =1.179-2.262, P = 0.003), while circulating ESM-1 levels have no significant correlation with the Gensini score. Furthermore, circulating ESM-1 showed higher discriminatory accuracy in predicting the presence of OSA (AUC:0.910).ConclusionsCirculating ESM-1 might function as a useful biomarker for monitoring the development and progression of CAD in OSA patients.
| S-EPMC6701084 | biostudies-literature
Project description:BackgroundObstructive sleep apnea (OSA) is common and independently associated with heart failure. This study aimed to investigate the impact of OSA on heart function in patients with dilated cardiomyopathy (DCM) as well as the possible mechanism related to exosomes regulated autophagy.Methods and resultsA total of 126 patients with DCM who underwent sleep evaluations were analyzed retrospectively. Cardiomyocytes were treated with exosomes isolated from untreated OSA patients and healthy controls. Fibrotic and hypertrophic markers were evaluated, and Akt/mTOR pathway-mediated autophagy was investigated. DCM patients with severe OSA had larger right ventricular end-diastolic diameter (RVEDd) and right atrial diameter (RAD) and increased N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels than DCM patients without OSA. Moreover, NT-proBNP and diabetes mellitus were independently correlated with the apnea-hypopnea index in multiple linear regression analysis. Treatment with OSA-derived exosomes significantly increased Col1A1, ANP, and BNP protein expression and decreased the expression of the autophagy markers LC3B II/I and beclin1. Rapamycin treatment significantly increased the decreased autophagy markers and attenuated the increased expression of Col1A1, ANP and BNP induced by OSA-derived exosomes.ConclusionThe severity of OSA is significantly associated with cardiac injury and remodeling. The underlying mechanism may be related to changed autophagy levels, which are regulated by circulating exosomes via the Akt/mTOR signaling pathway. This study may provide a new clue for the treatment of heart failure with OSA.
| S-EPMC8936144 | biostudies-literature
Project description:A critical link between amyloid-beta (Aβ) and hypoxia has been demonstrated in in vitro and animal studies but has not yet been proven in humans. Obstructive sleep apnea syndrome (OSAS) is a common disorder that is characterized by nocturnal intermittent hypoxaemia. This study sought to examine the association between the chronic intermittent hypoxia and Aβ in OSAS patients. Forty-five cognitively normal OSAS patients and forty-nine age- and gender-matched subjects diagnosed with simple snoring and not OSAS were included in the present study. Serum Aβ40, Aβ42, total tau and phosphorylated tau 181 (P-tau 181) levels were measured using ELISA kits. All subjects were evaluated with nighttime polysomnography and cognitive tests. Compared with the controls, the OSAS patients exhibited significantly higher serum Aβ40, Aβ42 and total Aβ levels, and each of these levels was positively correlated with the apnea-hypopnea index, the oxygen desaturation index, and the mean and lowest oxyhaemoglobin saturations in the OSAS patients. Moreover, the OSAS patients exhibited strikingly higher serum P-tau 181 levels, and these levels were positively correlated with serum Aβ levels. This study suggests that there is an association between chronic intermittent hypoxia and increased Aβ levels, implying that hypoxia may contribute to the pathogenesis of Alzheimer's disease.
| S-EPMC4563592 | biostudies-literature
Project description:Carpal tunnel syndrome (CTS) is the most common entrapment neuropathy of the upper extremity. It is usually associated with the compression of the median nerve in the median groove. Because the main symptoms of CTS pain and numbness worsen at night, sleep disorders in CTS patients and the impact of preferred sleeping position on CTS development have been formerly studied. However, to the best of our knowledge, this is the first study assessing the frequency of CTS in obstructive sleep apnea (OSA) patients. This study aimed to determine the frequency of CTS in OSA patients and evaluate the causative relation between the two diseases.Records of individuals who were admitted to our sleep laboratory were retrospectively scanned. Eighty patients who were diagnosed with OSA and did not have comorbidities that might cause OSA (e.g., diabetes mellitus, hypothyroiditis, rheumatic diseases, and cervical radiculopathy) were included in the study along with 80 healthy controls who matched for age, sex, and BMI of OSA patients. To maintain observer blindness, patients were not questioned regarding their symptoms or the clinical data that would be used in the study. All participants underwent nerve conduction studies. Those who were diagnosed with CTS were questioned regarding CTS symptoms and the preferred sleeping position. Subsequently, patients were given the Boston CTS questionnaire.CTS frequency in OSA patients was found to be 27.5%. There was no significant relation between preferred sleeping position or being a manual worker and having CTS.CTS frequency in OSA patients is significantly higher than that in healthy individuals. In contrast to previous studies that have been performed in the absence of polysomnographic and electrophysiological data, in our study biomechanical factors were not associated with CTS presence. Therefore, we conclude that intermittent hypoxemia is the main etiological factor for CTS in OSA patients. Inflammation may be a common factor for etiopathogenesis for both diseases, but this hypothesis needs further investigation.
| S-EPMC5758072 | biostudies-other
Project description:Plasmatic microRNA sequencing was conducted in specific matched subgroups of subjects (n = 53) with and without OSA using HTG EdgeSeq miRNA WTA Assay technology.
2024-04-01 | GSE229362 | GEO
Project description:Background:Obstructive sleep apnea (OSA) is a common disease. It can cause many serious complications. OSA may increase the risk of hypertension. However, the exact mechanism of OSA causing hypertension is not fully understood. YKL-40/chitinase-3-like protein-1 plays an important role in vascular injury, repair, and generation. We sought to explore the role of YKL-40 in endothelial dysfunction and hypertension in OSA patients. Methods:All subjects were examined by polysomnography (PSG) and the expression of YKL-40 in the plasm of the subjects was measured by luminex. Carotid intima-media thickness (CIMT) was measured by B-mode ultrasound. Results:According to the conditions of OSA and hypertension, we studied four groups of 157 subjects, including OSA group (OSA, N=77), OSA with hypertension group (OSA+HT, N=37), hypertension group (HT, N=20), and healthly group (Con, N=23). YKL-40 levels were significantly elevated in OSA, OSA+HT, and HT group compared to Con groups. We used the ROC to predict the sensitivity and specificity of YKL-40 in all OSA patients or all hyperpietic patients. For OSA patients, the AUC of YKL-40 is 0.807 (95% confidence interval 0.725-0.888; p<0.01). For hyperpietic patients, the AUC of YKL-40 is 0.656 (95% confidence interval 0.570-0.742, p=0.01). There was a significant correlation between the parameter of OSA and hypertension and YKL-40 (P<0.05) and a significant correlation between Max-CIMT and YKL-40 (P<0.05). Conclusion:Elevated circulating levels of YKL-40 are associated with hypertension in OSA patients. The specificity of YKL-40 suggests that it could be a potential biomarker for OSA and hypertension.
| S-EPMC6436335 | biostudies-literature