Circulating Survivin Levels in Obstructive Sleep Apnoea

Kunos, László; Horváth, Péter; Kis, Adrián; Tárnoki, Dávid László; Tárnoki, Ádám Domonkos; Lázár, Zsófia; Bikov, András

doi:10.1007/s00408-018-0120-z

Cited by 13 publications

(15 citation statements)

References 43 publications

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“…However, the cleavage of uPAR may be slower in OSA due to decreased levels of uPA [8] and plasmin [5,6,23]. The expression of uPA is induced by female sexual hormones [20] and the proto-oncogenic survivin [27], which presented decreased expressions in OSA [3,28]. Plasmin is formed by plasminogen, and this reaction is blocked by plasminogen activator-inhibitors (PAI), shown to be upregulated in OSA [5,6,23].…”

Section: Discussionmentioning

confidence: 99%

“…Inpatient polysomnography and cardiorespiratory polygraphy were performed as described previously [2][3][4] using Somnoscreen Plus Tele PSG (Somnomedics GMBH Germany). Sleep stages, movements and cardiopulmonary events were scored manually according to the American Academy of Sleep Medicine [24] guidelines.…”

Section: Sleep Studiesmentioning

confidence: 99%

“…Chronic intermittent hypoxia and increased sympathetic tone induce production of pro-inflammatory molecules, such as interleukin (IL)-6, IL-1β, tumour necrosis factor-α [1] or complement elements [2] and suppresses the release of anti-inflammatory [3,4] molecules. Linked to inflammation and sympathetic activity, OSA is characterised by a hypercoagulation state [5][6][7][8][9].…”

Section: Introductionmentioning

confidence: 99%

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Circulating Soluble Urokinase-Type Plasminogen Activator Receptor in Obstructive Sleep Apnoea

et al. 2020

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Background and Objectives: Obstructive sleep apnoea (OSA) is associated with heightened systemic inflammation and a hypercoagulation state. Soluble urokinase-type plasminogen activator receptor (suPAR) plays a role in fibrinolysis and systemic inflammation. However, suPAR has not been investigated in OSA. Materials and Methods: A total of 53 patients with OSA and 15 control volunteers participated in the study. Medical history was taken and in-hospital sleep studies were performed. Plasma suPAR levels were determined by ELISA. Results: There was no difference in plasma suPAR values between patients with OSA (2.198 ± 0.675 ng/mL) and control subjects (2.088 ± 0.976 ng/mL, p = 0.62). Neither was there any difference when patients with OSA were divided into mild (2.134 ± 0.799 ng/mL), moderate (2.274 ± 0.597 ng/mL) and severe groups (2.128 ± 0.744 ng/mL, p = 0.84). There was no significant correlation between plasma suPAR and indices of OSA severity, blood results or comorbidities, such as hypertension, diabetes, dyslipidaemia or cardiovascular disease. Plasma suPAR levels were higher in women when all subjects were analysed together (2.487 ± 0.683 vs. 1.895 ± 0.692 ng/mL, p < 0.01), and also separately in controls (2.539 ± 0.956 vs. 1.411 ± 0.534 ng/mL, p = 0.02) and patients (2.467 ± 0.568 vs. 1.991 ± 0.686 ng/mL, p < 0.01). Conclusions: Our results suggest that suPAR does not play a significant role in the pathophysiology of OSA. The significant gender difference needs to be considered when conducting studies on circulating suPAR.Medicina 2020, 56, 77 2 of 10 Soluble urokinase-type plasminogen activator receptor (suPAR) is a molecule which plays a role in both inflammation and coagulation. It is produced upon cleavage of the membrane-bound urokinase-type plasminogen activator receptor (uPAR). The cleavage is facilitated by urokinase-type plasminogen activator (uPA), plasmin, matrix metalloproteases, neutrophil elastase and cathepsin G [11]. The urokinase receptor (also known as uPAR) is expressed by endothelial cells, macrophages, monocytes, neutrophils, lymphocytes, smooth muscle cells and fibroblasts [12,13]. It is upregulated under infections and as an effect of pro-inflammatory cytokines [11,[13][14][15], while suPAR contributes to plasminogen activation, cell adhesion, chemotaxis and immune cell activation [16]. However, uPAR also acts as a scavenger receptor for uPA, inhibiting its actions [17]. In large studies, plasma suPAR was elevated in coronary artery disease and cerebrovascular disease and correlated with their severity and cardiovascular mortality [18][19][20]. Higher suPAR levels were also observed in obesity [21], which is the main etiological factor for OSA in the Western population [22].Only one study has investigated suPAR in probable OSA so far [23]. Patients were categorised to high and low-risk OSA based on the Berlin questionnaire and neck circumferences; however, no objective sleep tests were performed. In this study, there was a tendency for higher suPAR levels in the high-risk group, but...

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Section: Discussionmentioning

confidence: 99%

Section: Sleep Studiesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Circulating Soluble Urokinase-Type Plasminogen Activator Receptor in Obstructive Sleep Apnoea

et al. 2020

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“…On the contrary, PSGL-1 is downregulated in apoptotic cells [19]. OSA is characterized by increased levels of pro-apoptotic [7] and decreased concentration of anti-apoptotic [20] molecules. The main receptor for PSGL-1 is P-selectin [21].…”

Section: Introductionmentioning

confidence: 96%

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

Horváth

Lázár

Gálffy

et al. 2020

Lung

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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.

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“…Obstructive sleep apnoea (OSA) is the most common sleep-related breathing disorder which is characterised by the repetitive collapse of the upper airways during sleep resulting in chronic intermittent hypoxaemia (CIH) and frequent arousals with sleep fragmentation. These factors lead to enhanced oxidative stress and consequential systemic inflammation which are associated with altered concentrations of circulating pro-inflammatory 1 , 2 and anti-inflammatory 3 , 4 biomarkers. Understanding the role of inflammation in OSA is of importance as it could be a link to the development of cardiometabolic comorbidities.…”

Section: Introductionmentioning

confidence: 99%

The role of hyaluronic acid and hyaluronidase-1 in obstructive sleep apnoea

Mészáros

Kis

Kunos

et al. 2020

Sci Rep

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Biological functions of hyaluronic acid (HA) depend on its molecular size. High-molecular weight HA (HMW-HA) is an important component of the endothelial wall and has anti-inflammatory and antioxidant properties. Under inflammation or hypoxia, HMW-HA is degraded by hyaluronidases, such as HYAL-1 resulting in pro-inflammatory low-molecular weight fragments. Obstructive sleep apnoea (OSA) is characterised by intermittent hypoxia and systemic inflammation. Our aim was to evaluate circulating HMW-HA and HYAL-1 in OSA. We recruited 68 patients with OSA and 40 control volunteers. After full-night sleep study blood samples were taken for HMW-HA and HYAL-1 measurements. HYAL-1 levels were significantly higher in patients with OSA compared to controls (0.59/0.31–0.88/ng/mL vs. 0.31/0.31–0.58/ng/mL; p = 0.005) after adjustment for gender, age, BMI and smoking. There was a trend for reduced HMW-HA concentrations in OSA (31.63/18.11–59.25/ng/mL vs. 46.83/25.41–89.95/ng/mL; p = 0.068). Significant correlation was detected between circulating HMW-HA and apnoea-hypopnoea-index (r = − 0.195, p = 0.043), HYAL-1 and apnoea-hypopnoea-index (r = 0.30, p < 0.01) as well as oxygen desaturation index (r = 0.26, p < 0.01). Our results suggest that chronic hypoxia is associated with increased plasma HYAL-1 concentration and accelerated HMW-HA degradation. Altered hyaluronan metabolism may be involved in the inflammatory cascade potentially leading to endothelial dysfunction in OSA.

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Circulating Survivin Levels in Obstructive Sleep Apnoea

Abstract: Plasma survivin levels are reduced in OSA, relate to disease severity, and are associated with high CRP levels. This suggests an impaired immunoregulation in this disorder which needs to be studied in further detail.

Cited by 13 publications

References 43 publications

Circulating Soluble Urokinase-Type Plasminogen Activator Receptor in Obstructive Sleep Apnoea

Circulating Soluble Urokinase-Type Plasminogen Activator Receptor in Obstructive Sleep Apnoea

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

The role of hyaluronic acid and hyaluronidase-1 in obstructive sleep apnoea

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