Effect of oral appliance on circulating leukocyte telomere length and SIRT1 in obstructive sleep apnea

Lin, Ching-Chi; Wang, Huey‐Yuan; Liaw, Shwu-Fang; Chiu, Chung-Hsin; Lin, Mei-Wei

doi:10.1007/s00784-018-2560-5

Cited by 21 publications

(14 citation statements)

References 35 publications

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“…One of the reports evaluated the usage of a mandibular advancement device in OSA individuals on markers of aging like LTL and sirtuin 1 (SIRT1), which is a signaling protein involved in metabolic regulation. It has been found that, after 3 months of the treatment, participants had longer LTL and higher levels of SIRT1 compared to the baseline results, suggesting that successful treatment of OSA can inhibit accelerated aging [32]. Similar results have been reported by Khalyfa et al, who also found increased SIRT1 expression after 12 months of continuous positive airway pressure (CPAP) treatment in OSA patients [33].…”

Section: Telomere Shortening In Osasupporting

confidence: 76%

Obstructive Sleep Apnea as an Acceleration Trigger of Cellular Senescence Processes through Telomere Shortening

Turkiewicz

Ditmer

Sochal

et al. 2021

IJMS

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Obstructive sleep apnea (OSA) is chronic disorder which is characterized by recurrent pauses of breathing during sleep which leads to hypoxia and its two main pathological sequelae: oxidative stress and chronic inflammation. Both are also associated with cellular senescence. As OSA patients present with higher prevalence of age-related disorders, such as atrial hypertension or diabetes mellitus type 2, a relationship between OSA and accelerated aging is observable. Furthermore, it has been established that these OSA are associated with telomere shortening. This process in OSA is likely caused by increased oxidative DNA damage due to increased reactive oxygen species levels, DNA repair disruptions, hypoxia, chronic inflammation, and circadian clock disturbances. The aim of the review is to summarize study outcomes on changes in leukocyte telomere length (LTL) in OSA patients and describe possible molecular mechanisms which connect cellular senescence and the pathophysiology of OSA. The majority of OSA patients are characterized by LTL attrition due to oxidative stress, hypoxia and inflammation, which make a kind of positive feedback loop, and circadian clock disturbance.

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Section: Telomere Shortening In Osasupporting

confidence: 76%

Obstructive Sleep Apnea as an Acceleration Trigger of Cellular Senescence Processes through Telomere Shortening

Turkiewicz

Ditmer

Sochal

et al. 2021

IJMS

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“…An association between Sirt2 and OSA during REM sleep has not previously been reported. There are, however, some studies of the closely related Sirt1 protein and OSA (Chen et al, 2015; Lin, Wang, Liaw, Chiu, & Lin, 2018). In patients with OSA, Sirt1 levels were lower than in healthy controls and, after CPAP treatment (Chen et al, 2015) or oral appliance treatment (Lin et al, 2018), the levels increased.…”

Section: Discussionmentioning

confidence: 99%

“…There are, however, some studies of the closely related Sirt1 protein and OSA (Chen et al, 2015; Lin, Wang, Liaw, Chiu, & Lin, 2018). In patients with OSA, Sirt1 levels were lower than in healthy controls and, after CPAP treatment (Chen et al, 2015) or oral appliance treatment (Lin et al, 2018), the levels increased. There are no previous studies of LAP‐TGF‐β 1 and OSA during REM sleep, and for OSA based on a whole night the results of previous studies are conflicting (Alberti et al, 2003; Hernandez‐Jimenez et al, 2017; Steffanina et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

Association between proteomics and obstructive sleep apnea phenotypes in a community‐based cohort of women

Ljunggren

Theorell‐Haglöw

Freyhult

et al. 2020

Journal of Sleep Research

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Proteomic-based technologies offer new opportunities to identify proteins that might reflect the cardiometabolic stress caused by different aspects of sleep-disordered breathing. We aimed to investigate whether severe obstructive sleep apnea and severe obstructive sleep apnea during rapid eye movement sleep are associated with changed levels of inflammatory and cardiac disease-related proteins in a populationbased cohort of women. In the community-based "Sleep and Health in Women" (SHE) cohort study, 400 women underwent polysomnography, anthropometric measurements and blood sampling. Two proteomic assays (Olink Proseek ® Inflammation panel and Olink Proseek ® Cardiovascular II panel), each measuring 92 proteins, were analysed in a subsample of 253 women. p-Values were adjusted for multiple testing, with false discovery rate set at 10%. In unadjusted models, 57 proteins were associated with apnea−hypopnea index, 56 proteins with oxygen desaturation index and 64 proteins with rapid eye movement−apnea−hypopnea index. After adjustment for age, body mass index and plate, there were no significant associations between apnea−hypopnea index or oxygen desaturation index and any of the proteins. Severe obstructive sleep apnea during rapid eye movement sleep (rapid eye movement− apnea−hypopnea index ≥ 30) was associated with decreased levels of two anti-inflammatory proteins; Sirt2 (q-value .016) and LAP-TGF-β 1 (q-value .016). There was also a negative association between rapid eye movement−apnea−hypopnea index of ≥ 30 and Axin1 (q-value .095), a protein thought to facilitate TGF-β-signalling. We conclude that severe obstructive sleep apnea during rapid eye movement sleep is associated with low levels of Sirt2, LAP-TGF-β 1 and Axin1, anti-inflammatory proteins involved in metabolic regulation and in the atherosclerotic process. For obstructive sleep apnea based on a whole night, the associations with cardiac and inflammatory proteins are weaker, and explained to a large extent by age and body mass index.

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“…Pathway analysis demonstrated that the 22 differentially expressed miRNAs are related to distinct molecular pathways associated with cellular senescence, cell cycle, adherens, tight junction, atherosclerosis, TGF-β signaling, TNF-α signaling, insulin resistance, Alzheimer’s disease, and HIF-1α signaling, all of which have been found to play a role in the development of adverse consequences of OSA. Accordingly, recent studies have shown that OSA may exacerbate vascular senescence via oxidative stress-related pathways through exosomes, accelerate chromosomal aging as evidenced by shortened telomere length, and trigger a senescence-like phenotype in pre-adipocytes [ 35 , 36 , 37 , 38 ]. Abnormal activity of the core cell-cycle machinery represents a driving force of tumorigenesis, while OSA has been recognized as a risk factor for cancer growth and aggressiveness mainly through HIF-1α signaling, which controls the synthesis of molecules with effects on inflammation, immune surveillance, and cell proliferation [ 39 ].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA Sequencing Analysis in Obstructive Sleep Apnea and Depression: Anti-Oxidant and MAOA-Inhibiting Effects of miR-15b-5p and miR-92b-3p through Targeting PTGS1-NF-κB-SP1 Signaling

Chen

Hsu

et al. 2021

Antioxidants

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The aim of this study was to identify novel microRNAs related to obstructive sleep apnea (OSA) characterized by intermittent hypoxia with re-oxygenation (IHR) injury. Illumina MiSeq was used to identify OSA-associated microRNAs, which were validated in an independent cohort. The interaction between candidate microRNA and target genes was detected in the human THP-1, HUVEC, and SH-SY5Y cell lines. Next-generation sequencing analysis identified 22 differentially expressed miRs (12 up-regulated and 10 down-regulated) in OSA patients. Enriched predicted target pathways included senescence, adherens junction, and AGE-RAGE/TNF-α/HIF-1α signaling. In the validation cohort, miR-92b-3p and miR-15b-5p gene expressions were decreased in OSA patients, and negatively correlated with an apnea hypopnea index. PTGS1 (COX1) gene expression was increased in OSA patients, especially in those with depression. Transfection with miR-15b-5p/miR-92b-3p mimic in vitro reversed IHR-induced early apoptosis, reactive oxygen species production, MAOA hyperactivity, and up-regulations of their predicted target genes, including PTGS1, ADRB1, GABRB2, GARG1, LEP, TNFSF13B, VEGFA, and CXCL5. The luciferase assay revealed the suppressed PTGS1 expression by miR-92b-3p. Down-regulated miR-15b-5p/miR-92b-3p in OSA patients could contribute to IHR-induced oxidative stress and MAOA hyperactivity through the eicosanoid inflammatory pathway via directly targeting PTGS1-NF-κB-SP1 signaling. Over-expression of the miR-15b-5p/miR-92b-3p may be a new therapeutic strategy for OSA-related depression.

show abstract

Effect of oral appliance on circulating leukocyte telomere length and SIRT1 in obstructive sleep apnea

Abstract: LTL and SIRT1 protein levels in PBMC can be improved following effective treatment of OSA using MAD.

Cited by 21 publications

References 35 publications

Obstructive Sleep Apnea as an Acceleration Trigger of Cellular Senescence Processes through Telomere Shortening

Obstructive Sleep Apnea as an Acceleration Trigger of Cellular Senescence Processes through Telomere Shortening

Association between proteomics and obstructive sleep apnea phenotypes in a community‐based cohort of women

MicroRNA Sequencing Analysis in Obstructive Sleep Apnea and Depression: Anti-Oxidant and MAOA-Inhibiting Effects of miR-15b-5p and miR-92b-3p through Targeting PTGS1-NF-κB-SP1 Signaling

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