Serum YKL–40/chitinase 3–like protein 1 level is an independent predictor of atherosclerosis development in patients with obstructive sleep apnea syndrome

Bakırcı, Eftal Murat; Ünver, Edhem; Değirmenci, Hüsnü; Kıvanç, Tülay; Günay, Murat; Hamur, Hikmet; Büyüklü, Mutlu; Ceyhun, Gökhan; Topal, Ergün; Çoban, Taha Abdulkadir

doi:10.5543/tkda.2015.56805

Cited by 10 publications

(10 citation statements)

References 8 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, Chi3l1 was found to be secreted from differentiated macrophages in early-stage atherosclerosis lesions 59 , 60 as well as from VSMCs during hyper cholesterol-induced coronary atherosclerotic plaque development in swine 31 . Notably, knockdown of the elevated Chi3l1 expression associated with the atherosclerotic aorta and endothelial dysfunction suppresses the progression of these characteristics in a mouse model 30 - 32 , 34 , 38 , 61 . These data suggest that in addition to its potential role as a circulating biomarker for AD diagnosis 24 - 29 , Chi3l1 might play an important role in vascular inflammation and the development of atherosclerosis in patients with AD.…”

Section: Discussionmentioning

confidence: 99%

Atherosclerosis is exacerbated by chitinase-3-like-1 in amyloid precursor protein transgenic mice

Jung¹,

Kim²,

Park³

et al. 2018

Theranostics

View full text Add to dashboard Cite

Although the important role of amyloid precursor protein (APP) in vascular diseases associated with Alzheimer's disease (AD) has been demonstrated, the underlying molecular mechanisms and physiological consequences are unclear. We aimed to evaluate vascular inflammation and atherosclerosis in Swedish mutant of human APP transgenic (APPsw-Tg) and ApoE-/-/APPsw-Tg mice. We also aimed to explore the mechanisms underlying any changes observed in these mice compared with non-Tg controls. Methods: The transgenic and non-Tg mouse strains were subjected to partial ligation of the left carotid artery to induce atherosclerotic changes, which were measured using histological approaches, immunohistochemistry, quantitative polymerase chain reaction, and gene expression microarrays. Results: Our results showed increased vascular inflammation, arterial wall thickness, and atherosclerosis in APPsw-Tg and ApoE-/-/APPsw-Tg mice. We further found that the expression of chitinase-3-like-1 (Chi3l1) is increased in the APPsw-Tg mouse artery and Chi3l1 mediates endothelial cell (EC) inflammation and vascular smooth muscle cell (VSMC) activation, which in turn exacerbates atherosclerosis. In addition, using two publicly available microarray datasets from the dorsolateral prefrontal cortex of people with AD and unaffected controls as well as inflamed human umbilical vein endothelial cells, we found that Chi3l1 and associated inflammatory gene were significantly associated with AD, evaluated by co-expression network analysis and functional annotation. Knockdown of Chi3l1 in the arterial endothelium in vivo suppressed the development of atherosclerosis. We also show that microRNA 342-3p (miR-342-3p) inhibits EC inflammation and VSMC activation through directly targeting Chi3l1, and that APPsw increased Chi3l1 expression by reducing miR-342-3p expression in the arterial endothelium, promoting atherosclerosis. Conclusion: Our findings suggest that targeting Chi3l1 might provide new diagnostic and therapeutic strategies for vascular diseases in patients with AD.

show abstract

Section: Discussionmentioning

confidence: 99%

Atherosclerosis is exacerbated by chitinase-3-like-1 in amyloid precursor protein transgenic mice

Jung¹,

Kim²,

Park³

et al. 2018

Theranostics

View full text Add to dashboard Cite

show abstract

“…Several studies have reported elevated YKL-40 levels in different cardiovascular conditions and it has been described a positive association between this marker and mortality [ 10 – 17 ]. It has been reported an increased YKL-40 expression in patients with carotid atherosclerosis [ 18 ], as well as a positive correlation between common carotid artery intima media thickness (CIMT) and YKL-40 levels in patients with obstructive sleep apnea syndrome [ 16 ] and between arterial stiffness and YKL-40 levels in essential hypertension subjects [ 15 ]. Increased YKL-40 levels have also been found both in patients with T1D and T2D [ 19 – 22 ], and particularly in T1D and T2D patients with microalbuminuria, suggesting that this glycoprotein might be used as an early marker of vascular disease [ 18 , 21 ].…”

Section: Introductionmentioning

confidence: 99%

Relationship of YKL-40 and adiponectin and subclinical atherosclerosis in asymptomatic patients with type 1 diabetes mellitus from a European Mediterranean population

Aguilera

Serra-Planas

Granada

et al. 2015

Cardiovasc Diabetol

View full text Add to dashboard Cite

BackgroundThe glycoprotein YKL-40 is a new marker of early inflammation and endothelial dysfunction. Adiponectin is a collagen-like protein with anti-atherogenic and anti-inflammatory effects. Increased concentrations of both markers have been reported in patients with type 1 diabetes (T1D).AimTo assess the possible role of YKL-40 and adiponectin as a marker of subclinical cardiovascular disease in asymptomatic patients with type 1 diabetes with no history of ischemic or macrovascular heart disease and its relationship with other classic inflammatory biomarkers.MethodsConcentrations of YKL-40, adiponectin, IL-6, IL-1β, TNF- α, hsCRP and homocysteine were determined in 150 T1D patients (58 % men, age: 38.6 ± 8.1 years, 20.4 ± 8.1 years of evolution, BMI: 25.1 ± 3.6 kg/m2; HbA1c 8.1 ± 2.3 %, 48 % smokers; 26 % retinopathy, microalbuminuria 9 %) and 50 controls age, sex and smoke condition matched. Subclinical atherosclerosis was assessed by a carotid ultrasonography and a computed tomography for evaluation of calcium artery calcification score (CACS).Results82 % of T1D patients and 92 % of controls had a calcium score of 0. T1D patients showed a significantly higher mean common carotid artery intima media thickness (CIMT) compared to controls (0.55 ± 0.14 vs 0.48 ± 0.14 mm, p = 0.01). Concentrations of YKL-40 and adiponectin were significantly higher in T1D [42.6 (10.4–195.0) vs ±28.7 (11.0–51.2) ng/ml, p = 0.001 and 15.8 ± 9.1 vs. 12.4 ± 5.3 mg/ml, p = 0.008], with no differences when compared to other inflammatory parameters. In T1D patients no association was found between YKL-40 and adiponectin and screening test for subclinical arterial disease (neither CACS nor CIMT). A positive correlation was found between levels of YKL-40 and age and duration of disease (r = 0.28, p = 0.003; r = 0.35, p = 0.001). There were no differences in the YKL-40 in relation to the presence or absence of retinopathy or nephropathy. Levels of adiponectin were higher in patients with nephropathy (21.84 ± 8.15 vs. 14.88 ± 8.27 mg/ml, p = 0.008).ConclusionsType 1 diabetes patients from a Mediterranean area with a longer disease evolution, although a lower degree of subclinical disease, showed significatively higher concentrations of YKL-40 and adiponectin compared with the controls. Therefore, we conclude that YKL-40 and adiponectin are early inflammatory markers in diabetic subjects even in the presence of a low atherosclerotic background.

show abstract

“…In this study, the absence of DLCO elevation could be attributed to the association of two opposite mechanisms occurring during OSAS: (i) an increase in pulmonary capillary blood volume due to obesity and an increase in cardiac output linked to the hyperactivity of the sympathetic system, this latter tends to increase the DLCO; (ii) an alteration of the alveolar-capillary membrane which tends to reduce the DLCO. Indeed, during the course of OSAS in obese patients, an increase in the atherosclerosis and the inflammatory manifestations causing an alteration of the pulmonary exchanger was often noted [14,15,41]. e degree of bronchial inflammation was significantly greater in the OSAS group than the control group.…”

Section: Discussionmentioning

confidence: 99%

The Ventilatory and Diffusion Dysfunctions in Obese Patients with and without Obstructive Sleep Apnea-Hypopnea Syndrome

et al. 2020

View full text Add to dashboard Cite

Objective. To analyze the ventilatory and alveolar-capillary diffusion dysfunctions in case of obesity with or without an OSAS. Methods. It is a cross-sectional study of 48 obese adults (23 OSAS and 25 controls). Anthropometric data (height, weight, and body mass index (BMI)) were collected. All adults responded to a medical questionnaire and underwent polysomnography or sleep polygraphy for apnea-hypopnea index (AHI) and percentage of desaturation measurements. The following lung function data were collected: pulmonary flows and volumes, lung transfer factor for carbon monoxide (DLCO), and fraction of exhaled nitric oxide (FeNO). Results. Obesity was confirmed for the two groups with a total sample mean value of BMI = 35.06 ± 4.68 kg/m2. A significant decrease in lung function was noted in patients with OSAS compared with controls. Indeed, when compared with the control group, the OSAS one had a severe restrictive ventilatory defect (total lung capacity: 93 ± 14 vs. 79 ± 12%), an abnormal DLCO (112 ± 20 vs. 93 ± 22%), and higher bronchial inflammation (18.40 ± 9.20 vs. 31.30 ± 13.60 ppb) (p<0.05). Conclusion. Obesity when associated with OSAS increases the severity of pulmonary function and alveolar-capillary diffusion alteration. This can be explained in part by the alveolar inflammation.

show abstract

Serum YKL–40/chitinase 3–like protein 1 level is an independent predictor of atherosclerosis development in patients with obstructive sleep apnea syndrome

Abstract: In patients with OSAS, CIMT was increased. This increase was associated with serum YKL-40 level. Increased serum level of YKL-40 may be an early predictor of atherosclerosis development in patients with OSAS.

Cited by 10 publications

References 8 publications

Atherosclerosis is exacerbated by chitinase-3-like-1 in amyloid precursor protein transgenic mice

Atherosclerosis is exacerbated by chitinase-3-like-1 in amyloid precursor protein transgenic mice

Relationship of YKL-40 and adiponectin and subclinical atherosclerosis in asymptomatic patients with type 1 diabetes mellitus from a European Mediterranean population

The Ventilatory and Diffusion Dysfunctions in Obese Patients with and without Obstructive Sleep Apnea-Hypopnea Syndrome

Contact Info

Product

Resources

About