Archives

  • 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • 2020-02
  • 2020-03
  • 2020-04
  • 2020-05
  • 2020-06
  • 2020-07
  • 2020-08
  • 2020-09
  • 2020-10
  • 2020-11
  • 2020-12
  • 2021-01
  • 2021-02
  • 2021-03
  • 2021-04
  • 2021-05
  • 2021-06
  • 2021-07
  • 2021-08
  • 2021-09
  • 2021-10
  • 2021-11
  • 2021-12
  • 2022-01
  • 2022-02
  • 2022-03
  • 2022-04
  • 2022-05
  • 2022-06
  • 2022-07
  • 2022-08
  • 2022-09
  • 2022-10
  • 2022-11
  • 2022-12
  • 2023-01
  • 2023-02
  • 2023-03
  • 2023-04
  • 2023-05
  • 2023-06
  • 2023-07
  • 2023-08
  • 2023-09
  • 2023-10
  • 2023-11
  • 2023-12
  • 2024-01
  • 2024-02
  • 2024-03
  • The findings from this study

    2018-11-05

    The findings from this study extend what is known about the urinary proteome in OSA and severe obesity. Using CE–MS, we previously observed a panel of peptides in a study of severely obese subjects with and without OSA [16]. In the present study, the characterised urinary proteome with CPAP comprised a similar make-up of collagens and a peptide related to fibrinogen. Additionally, one peptide for which no sequence data is as yet available was found to be present in the peptide panel in both studies. The nature of peptides that constitute both panels may relate to the underlying vascular changes present in OSA including sympathetic activation, oxidative stress and inflammation [6]. In this study, the majority of the identified peptides were fragments of collagen alpha-1 (I) and (III) in addition to fibrinogen beta chain and cadherin 13 (T-Cadherin) peptides. Fibrinogen beta chain has a role in fibrinogen synthesis and haemostasis, blood viscosity as a binding surface for proteins and as an extracellular matrix component, and may be associated with cardiovascular risk factors [28]. T-Cadherin is highly expressed in the vasculature including endothelial cells, has been implicated in the modulation of angiogenic activities and is associated with circulating levels of adiponectin that is important for vascular homoeostasis. Additionally, links between T-cadherin and blood pressure, lipids, metabolic syndrome, type 2 diabetes and ischaemic stroke have been found in genome-wide association studies [29]. It should be noted that the mean amplitude of fibrinogen beta chain and cadherin-13 was lower in the CPAP-treated patients and it is possible that this may reflect decreased breakdown or differential expression with treatment. The extracellular matrix contains a fibrillar collagen network that is regulated by fibroblasts and myofibroblasts. Changes in vasoactive peptides and proinflammatory cytokines, and activity of Wnt agonist 1 that process procollagen precursors to mature collagen including procollagen proteinases and collagen degradation enzymes (matrix metalloproteinases) may account for the excretion of urinary collagen fragments [30]. Furthermore, it is known that alterations of the myocardial collagen matrix may occur in cardiovascular disease that may result in perturbations in vascular function [30]. In this context, it is known that OSA is associated with cardiovascular disease [31], and the peptides in the peptide panel may be a reflection of underlying cardiovascular changes associated with CPAP. The mechanisms underlying the observed urinary peptide profile in this study remain unclear, but may be related to the treatment effects of CPAP on intermittent hypoxia and systemic hypertension. Post-translational modification of proteins has been postulated as a mechanism by which protein function is influenced by chronic intermittent hypoxia, and there is evidence that this induces changes in the phosphorylation state of proteins associated with transcriptional activation, signal transduction pathways, and neurotransmitter synthesis [32]. Multiple lines of evidence underscore the importance of CPAP treatment in lowering BP in patients with severe OSA [33]. Additionally, OSA-mediated hypertension may be influenced by the effects of CPAP on reducing renin-angiotensin system activity with changes in renal perfusion [17,18]. It is conceivable that the treatment effects of CPAP on OSA disease progression may lead to the modification of proteins and changes in protease activity, and renal effects that may be reflected in the urinary proteome [15].
    Conclusion
    Funding This research was supported by the University of Liverpool, St Helens and Knowsley Hospital and University Hospital Aintree, United Kingdom (Grant nos. JXR 10169 and JXR 10170).
    Conflict of interest statement
    Contribution
    Acknowledgements
    Introduction People who sleep well, based on their own needs and in free conditions (weekends, vacation), feel alert during the day, rested, and in an optimal state to perform their daily activities. However, when they suffer a reduction of sleep due to work, school or social activities, physiological and cognitive changes occur that affect their physical and mental health [1,2]. Currently, the majority of the population suffers from chronic partial sleep deprivation [3], so it is important to analyze the effects of sleep reduction on human performance [4,5].