Liver X Receptor Gene Expression is Enhanced in Children with Obstructive Sleep Apnea-Hyperpnoea Syndrome and Cyclooxygenase-2 (COX-2) is Correlated with Severity of Obstructive Sleep Apnea-Hypopnea Syndrome (OSAHS)

Abstract

BackgroundLiver X receptor (LXR) is a nuclear receptor presenting in macrophages; it works indispensably in lipid metabolism control and also negatively regulates the expression of inflammatory genes in macrophages. There are many LXR-related studies in adults with metabolic syndrome but rare reports in obese children with obstructive sleep apnea-hypopnea syndrome (OSAHS). The aim of this study was to investigate the expression of LXR, cholesterol ester transfer protein (CETP), and cyclooxygenase-2 (COX-2) genes in obese children with OSAHS compared with obese children without OSAHS and non-obese children.Material/MethodsSleep monitoring was conducted in 80 obese children with sleep disorders. Fasting morning blood samples from the 80 obese children and 51 normal children were collected and separated, so that macrophages were obtained after culture. Fluorescence quantitative real-time PCR (RT-PCR) was used to detect expression levels of the LXR, CETP, and COX-2 genes.ResultsLXR, COX-2, and CETP levels in the OSAHS group were higher than those in the other two groups (P<0.05), and the LXR levels in the group of obese children without OSAHS were higher than those in control group (P<0.05). COX-2 expression in the group with moderate to severe OSAHS was higher than that in the group with mild OSAHS (P<0.05). Meanwhile, there were no significant differences in the LXR and CETP levels between the moderate to severe OSAHS group and the mild OSAHS group (P>0.05).ConclusionsLXR gene expression was significantly increased in obese children with OSAHS. The severity of OSAHS was positively correlated with COX-2 levels.

LncRNA XIST promotes inflammation by downregulating GRα expression in the adenoids of children with OSAHS

“…According to the apnea-hypopnea index, the patients were diagnosed with OSAHS when apnea-hypopnea occurred ≥ one time per hour, as previously described (23) Cell cultures. Human nasopharyngeal epithelial cell line NP69 purchased from American Type Culture Collection (ATCC) was cultured in keratinocyte-SFM medium (Invitrogen; Thermo Fisher Scientific, Inc.).…”

“…According to the apnea-hypopnea index, the patients were diagnosed with OSAHS when apnea-hypopnea occurred ≥ one time per hour, as previously described ( 23 ). Adenoid tissue specimens were collected from children with OSAHS (n=26) and healthy donors (n=21) with myocarditis at the Department of Otorhinolaryngology, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, from May 2017 to May 2018.…”

The Genetics of Sleep Disorders in Children: A Narrative Review

“…The link between OSA in children and being overweight can be explained by different mechanisms. Children with OSA have been reported to have an increased expression of the Liver X receptors (LXRs), nuclear receptors that play a central role in the transcriptional control of lipid metabolism [53], as well as higher plasma fatty-acid binding protein 4, a cytosolic protein abundantly expressed in adipocytes and macrophages [54]. Contrasting data have been reported on the association between OSA and Apolipoprotein E (APOE) gene [47].…”

The Role of Cyclooxygenase Enzymes and Microparticles in Obstructive Sleep Apnea Related Cerebrovascular Incidents

“…[3] Cyclooxygenase has 2 isoenzymes, namely COX-1 and COX-2, both of which are important mediators in the inflammatory response and vital regulators in peripheral blood vessels. [4,5] The increased risk of cerebral and peripheral vascular disease which is associated with Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) and selective COX-2 inhibitors emphasizes the importance of prostanoids in vascular regulation. Although nonselective and selective inhibition of COX-2 increase the risk of cardiovascular and cerebrovascular disease, there is still considerable controversy regarding the important role of COX-1 and COX-2 in forming prostanoids for vascular regulation.…”