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Abstract Background Previous studies demonstrated that the transforming growth factor (TGF) β superfamily, including TGF-βs and bone morphogenetic proteins (BMPs), plays important roles in cardiovascular diseases. The kielin/chordin-like protein (KCP) is a secreted protein that regulates the expression and function of TGF-βs and BMPs. However, the role of KCP during heart failure (HF) remains unknown. The present study aimed to investigate the cardiac expression of KCP in human failing hearts. Methods The human failing heart samples from patients with dilated cardiomyopathy (DCM, n = 12) and ischemic cardiomyopathy (ICM, n = 12) were collected, and normal heart (n = 8) samples from unmatched donors were collected as controls. Collagen volume, KCP levels, and mRNA levels of several BMPs in left ventricles (LV) of all hearts were measured. Results The KCP levels were significantly higher in human failing hearts than in normal hearts. KCP levels were positively associated with hypertrophy markers, including atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and β-myosin heavy chain (β-MHC). In addition, KCP levels were also positively associated with left ventricular end-diastolic dimension (LVEDD), collagen Iα and collagen IIIα expression but were negatively associated with left ventricular ejection fraction (LVEF). Furthermore, increased TGF-β1, BMP2/4/6/10 and reduced BMP7 levels were observed, and positive correlations between KCP and TGF-β1 and negative correlation between KCP and BMP2/7 were found, but not for BMP4/6/10. Conclusions KCP was closely associated with heart failure. The regulation of BMP2/7 and TGF-β1 expression may be the possible mechanisms. Highlights • KCP increases in human failing hearts when compare with normal hearts. • KCP is associated with the severity of heart failure. • KCP may participate in HF by regulating BMP2/7 and TGF-β1 level. [ABSTRACT FROM AUTHOR]

Abstract Background Interleukin (IL)-22 plays important roles in the development of arterial disease, including atherosclerosis and hypertension. However, the relationship between IL-22 and acute thoracic aortic dissection (TAD) remains unknown. Methods Blood samples were collected from patients with chest pain who underwent computed tomography angiography of the thoracic aorta but had no known preoperative diagnosis of coronary artery disease, peripheral artery disease, arthritis, and/or membranous nephropathy. Patients were divided into non-AD (NAD) and TAD groups, and the plasma concentrations of IL-22, IL-6 and tumor necrosis factor (TNF)-α were measured. In addition, aortic tissue samples from acute TAD patients and normal donors were collected, and the expression levels of IL-22 and IL-22 receptor 1 (IL-22R1) were measured. Results IL-22, IL-6 and TNF-α levels were significantly higher in acute TAD patients than in NAD patients (IL-22, NAD group: 27.0 (19.1, 38.6) pg/ml vs. TAD group: 32.9 (20.6, 58.3) pg/ml, p < 0.0001). The correlation analysis showed that IL-22 levels were positively correlated with levels of IL-6, TNF-α, fasting glucose, blood pressure, white blood cells, C-reactive proteins and D-dimers. Binary logistic regression analyses showed that IL-22 was independently associated with the presence of acute TAD (OR 1.169, 95% CI 1.069 to 1.277; p = 0.001). In addition, compared with aortic tissue of normal controls, TAD aortas showed increased expression of IL-22 and IL-22R1, especially in the torn section (IL-22, non-torn section: 2.8 ± 0.5/HPF vs. torn section 2.8 ± 0.5/HPF, p < 0.001). Additionally, macrophage but not T lymphocyte infiltration was significantly increased in the torn section (Macrophage, non-torn section: 2.2 ± 0.6/HPF vs. torn section 5.7 ± 1.2/HPF, p < 0.001; T lymphocyte, non-torn section: 2.7 ± 0.9/HPF vs. torn section 2.4 ± 0.5/HPF, p = 0.28), as evidenced by increased positive staining for the macrophage marker CD68, as opposed to the T cell marker CD3. Conclusion IL-22 levels may correlate with the presence of acute TAD. Highlights • IL-22 expression was significantly increased both in the plasma and aortas of TAD. • IL-22 was independently associated with the presence of acute TAD and regulation of inflammation was the possible mechanism. • IL-22 may be a new biomarker for TAD and be useful for the diagnosis of TAD. [ABSTRACT FROM AUTHOR]

Background Interleukin (IL) 11 is closely related to tumor and hematological system diseases. Recent studies have demonstrated that IL-11 also participates in cardiovascular diseases, including ischemia-reperfusion mediated heart injury and acute myocardial infarction. This study aimed to investigate whether IL-11 is involved in acute thoracic aortic dissection (TAD). Methods Aortic tissue samples from normal donors and acute TAD patients were collected, and the expression of IL-11 in all aortic tissue was analyzed. In addition, blood samples from patients with chest pain were collected and divided into a non-AD (NAD) group and a TAD group according to the results of computed tomography angiography of the thoracic aorta. The plasma IL-11, IL-17 and interferon (IFN) γ in all blood samples were measured. Results Compared with aortic tissue of normal controls, IL-11 was significantly increased in aortic tissue of acute TAD patients, especially in the torn section. The IL-11 was derived from aorta macrophages in TAD. In addition, the plasma IL-11, IL-17 and IFN-γ were significantly higher in acute TAD patients than in NAD patients, and the correlation analysis showed that IL-11 levels were positively correlated with levels of IFN-γ, IL-17, glucose, systolic blood pressure, diastolic blood pressure, white blood cells, C-reactive proteins and D-dimers. Binary logistic regression analyses showed that elevated IL11 in patients who may have diagnostic value of TAD, but less that D-dimer. Conclusion IL-11 was increased in thoracic aorta and plasma of TAD patients and may be a promising biomarker for diagnosis in patients with TAD. [ABSTRACT FROM AUTHOR]

Background Sestrins (Sesns) family, which including three members Sesn1, Sesn2 and Sesn3, is known as stress-inducible proteins and participate in multiple diseases via regulating oxidative stress, inflammatory response and cell apoptosis. The present study aimed to investigate the plasma levels and the clinical significance of Sesns in patients with coronary artery disease (CAD). Methods In the case-control study, 119 CAD patients, including stable angina pectoris (SAP, n = 44), unstable angina pectoris (UAP, n = 41) and acute myocardial infarction (AMI, n = 29) were included. Patients with chest pain syndrome but excluded CAD (n = 35) were enrolled as control. Plasma levels of Sesn1, Sesn2, Sesn3, superoxide dismutase (SOD) and malondialdehyde (MDA) in all patients were measured and analyzed. Results Compared with control group, plasma levels of Sesn1, Sesn2 and Sesn3 were significantly increased in patients with SAP, UAP and AMI. In addition, a significant lower SOD levels and higher MDA levels were observed in CAD patients, Sesn1/2/3 levels were negatively correlated with SOD levels and positively correlated with MDA levels. Gensini Score were positively correlated with Sesn1/2/3 levels and MDA levels, whereas negatively correlated with SOD levels. Furthermore, as the main risk factors for CAD, the elderly and obesity increased plasma Sesn2 levels, diabetes increased both plasma Sesn2 and Sesn3 levels. Conclusions Our study was the first to report that the plasma Sesns levels were increased in CAD patients and positively related to the severity of coronary heart disease. Although the exact mechanisms of Sesns in CAD are still unknown, alleviated oxidative stress may be the possible reasons. [ABSTRACT FROM AUTHOR]