Xuerui Tan

Effects of osteopontin on functional activity of late endothelial progenitor cells

The aim of this study is to investigate the effect of osteopontin (OPN) on functional activity of late endothelial progenitor cells (EPCs). Total mononuclear cells (MNCs) were isolated from human umbilical cord blood by Ficoll density gradient centrifugation, and then the cells were plated on fibronectin‐coated culture plates. Late EPCs were positive for both 1,1‐dioctadecyl‐3,3,3,3‐tetramethylindocarbocyanine‐labeled acetylated low‐density lipoprotein (DiI‐acLDL) and fluorescein‐isothiocyanate‐conjugated Ulex europaeus agglutinin lectin (UEA‐1). Expression of von Willbrand factor (vWF) and kinase insert domain receptor (KDR) were detected by indirect immunofluorescence staining. Late EPCs of 3–5 passages were treated for 24 h with OPN (to make a series of final concentration: 0.005 µg/ml, 0.01 µg/ml, 0.05 µg/ml, 0.5 µg/ml, 2.5 µg/ml), or vehicle control. The proliferation, migration, and in vitro vasculogenesis activity of late EPCs were assayed by 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT) assay, modified Boyden chamber assay and an in vitro angiogenesis assay, respectively. Late EPCs adhesion assay was performed by replating cells on fibronectin‐coated plates, and then adherent cells were counted. Incubation with OPN dose‐dependently inhibited the proliferative, adhesive, and in vitro vasculogenesis capacity and increased migratory activity of late EPCs. J. Cell. Biochem. 112: 1730–1736, 2011.

Green tea may be benefit to the therapy of atrial fibrillation

Atrial fibrillation (AF) is the most common cardiac arrhythmia in clinical practice. Systemic inflammatory state, oxidative stress injury, and atrial fibrosis are identified as the main mechanisms for AF. Considering the multifactorial mechanisms of AF, a novel therapeutic agent with multi‐bioactivities should be presented. Regular consumption of green tea has been associated with a reduced risk of coronary heart disease and against a large number of pathologic conditions. Recent results indicate that green tea extract, especially (‐)‐epigallocatechin‐3‐gallate, could effectively decrease inflammatory factors secretion, antagonize oxidation, and inhibit matrix metalloproteinase activities. Inhibition of inflammation, modulation of oxidative stress, and targeting tissue fibrosis represent new approaches in tackling AF; therefore, green tea may be an innovative therapeutic candidate to prevent the occurrence, maintenance, and recurrence of AF. J. Cell. Biochem. 112: 1709–1712, 2011.

Atrial Fibrillation Is an Independent Risk Factor for Hospital-Acquired Pneumonia

Background Patients who were hospitalized for community-based pneumonia frequently had pre-existing atrial fibrillation (AF) and had subsequent cardiovascular complications. Whether patients who had AF would be susceptible to the development of hospital-acquired pneumonia (HAP) is a serious concern but this has not been investigated. In our clinics, we have made empirical observation of such susceptibility. Objectives To investigate the association between newly developed HAP and pre-existing AF, and to identify whether AF is an independent risk factor for HAP. Methods Hospital data from 8657 sequentially admitted inpatients [1059 patients with AF and 7598 without AF (NAF)] were collected from the Department of Cardiology, First Affiliated Hospital of Shantou University Medical College, Shantou, China, from January 1, 2009 to December 31, 2011. Exclusion criteria were: having previous or current pneumonia, pacemakers, sick sinus syndrome and repeated hospitalization. The incidence of HAP (within 48 hours after hospitalization) was identified among all the patients. Results Among the AF patients, 274 had HAP (adjusted rate 25.64%) which was significantly higher than the 276 NAF patients who had HAP (adjusted rate 3.66%; P<0.001). The increased risk was also associated with high blood pressure, heart failure and age, but not with gender, smoking, coronary heart disease, diabetes, congenital heart disease. In addition, our multiple regression analysis indicates that AF is an independent risk factor for HAP. Conclusion We have identified, for the first time, that AF is an important risk factor for HAP. Although additional clinical confirmation is needed, our data provide valuable evidence for use in prevention of HAP which is the most common cause of death from nosocomial infection.

Epigallocatechin-3-gallate inhibits proliferation of human aortic smooth muscle cells via up-regulating expression of mitofusin 2.

Previous studies have shown that epigallocatechin-3-gallate (EGCG) inhibits the proliferation of vascular smooth muscle cells (VSMCs) via the extracellular-signal-regulated kinase (ERK1/2) and mitogen activated protein kinases (MAPKs) pathway. Mitofusin 2 (Mfn-2) also suppresses VSMC proliferation through Ras-Raf-ERK/MAPK, suggesting a possible link between EGCG, Mfn-2 and ERK/MAPK. However, the effect of EGCG on Mfn-2 remains unknown. In this study, we investigated the role of Mfn-2 in the regulation of VSMC proliferation by EGCG, and assessed the underlying mechanisms. The effects of EGCG on the proliferation of cultured human aortic smooth muscle cells (HASMCs) were observed by 5-ethynl-2-deoxyuridine (EdU) incorporation assay. Mfn-2 gene and protein levels, and Ras, p-c-Raf and p-ERK1/2 protein levels were determined by quantitative real-time polymerase chain reaction and western blotting, respectively. Mfn-2 gene silencing was achieved by RNA interference. EGCG 50 μmol/L profoundly inhibited the proliferation of HASMCs in culture, up-regulated Mfn-2, and down-regulated the expression of p-c-Raf and p-ERK1/2. Furthermore, RNA interference-mediated gene knockdown of Mfn-2 antagonized EGCG-induced anti-proliferation and down-regulation of Ras, p-c-Raf and p-ERK1/2. These results suggest that EGCG inhibits the proliferation of HASMCs in vitro largely via Mfn-2-mediated suppression of the Ras-Raf-ERK/MAPK signaling pathway.

Ghrelin Could be a Candidate for the Prevention of In-Stent Restenosis

Percutaneous coronary intervention is a revolutionary treatment for ischemic heart disease, but in-stent restenosis (ISR) remains a clinical challenge. Inflammation, smooth muscle proliferation, endothelial function impairment, and local thrombosis have been identified as the main mechanisms for ISR. Considering the multifactorial mechanisms of ISR, a novel therapeutic agent with multiple bioactivities is required. Ghrelin is a novel gut–brain peptide predominantly produced by the stomach, and has been shown to play a role in various cardiovascular activities, such as increasing myocardial contractility, improving cardiac output, and inhibiting ventricular remodeling, as well as attenuating cardiac ischemia-reperfusion injury. Recent studies have demonstrated that ghrelin effectively inhibits vascular inflammation and vascular smooth muscle cell proliferation, repairs endothelial cells, promotes vascular endothelial function, inhibits platelet aggregation, and exerts antithrombotic effects. These findings suggest that ghrelin may be an innovative therapeutic candidate for the prevention and treatment of ISR.

Effects of urotensin II on functional activity of late endothelial progenitor cells.

Urotensin II (UII) is a potent vasoactive cyclic peptide which has multiple effects on the cardiovascular system. However, the effects of UII on late endothelial progenitor cells (EPCs) are still unclear. The aim of the present study is to investigate whether UII influences the functional activity of late EPCs. Late EPCs were isolated from human umbilical cord blood by Ficoll density gradient centrifugation and treated with UII (10(-10), 10(-9), 10(-8), 10(-7) and 10(-6)M), or vehicle control. Expression of urotensin II receptor (UT) in late EPCs was confirmed by indirect immunofluorescence staining. Late EPCs proliferation, migration and in vitro vasculogenesis activity were assayed with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, transwell chamber assay, and matrigel tube formation assay. Late EPCs adhesive assay was performed by replating cells on fibronectin-coated dishes, and then adherent cells were counted. Incubation with UII increased the migratory, adhesive and in vitro vasculogenesis capacity and inhibited the proliferative activity of late EPCs. Furthermore, these UII-mediated effects on late EPCs were attenuated by pretreatment with the UT antagonist urantide. These findings indicate that UII may exert multiple effects on functional activity of late EPCs through UT.

Lipopolysaccharide Impaired the Functional Activity of Endothelial Colony-Forming Cells

Background: Recent studies have shown that endothelial progenitor cells (EPCs) contribute to lung repair after lipopolysaccharide (LPS)-induced lung injury and infusion of LPS decreased early EPCs in human peripheral blood. However, the effects of LPS on endothelial colony-forming cells (ECFCs) remain to be determined. Objective: To investigate possible effects of LPS on the functional activity of ECFCs. Methods: ECFCs were isolated from human umbilical cord blood and characterized. ECFCs at passages 3-5 were treated for 24 h with either LPS or vehicle control. Their viability, migration and in vitro vasculogenesis activity were assayed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, modified Boyden chamber and in vitro angiogenesis assays, respectively. ECFC adhesion was assessed by replating cells on fibronectin-coated dishes and subsequent counting of adherent cells. Results: Incubation with LPS dose-dependently inhibited the viable, migratory, adhesive and in vitro vasculogenesis capacity of ECFCs. Conclusion: LPS impaired the functional activity of ECFCs.

Two parameters reflect lipid-driven inflammatory state in acute coronary syndrome: atherogenic index of plasma, neutrophil–lymphocyte ratio

BackgroundAtherosclerosis is a systemic, lipid-driven immune-inflammatory disease.MethodsWe retrospectively reviewed institutional electronic medical records to seek chest pain patients who were suspicious of acute coronary syndrome (ACS) between January 2011 and December 2013. All the patients were identified by undergoing coronary angiography. On admission white blood cell and its subtypes were measured as part of the automated complete blood count and fasting venous blood samples were obtained and analyzed for lipids profiles used automated analysis.ResultsA total of 376 consecutive patients with ACS were investigated. In the same period, 378 patients admitted with chest pain suspicious of ACS were also included in this study for control. Blood glucose, serum creatinine, white blood cell, neutrophil and monocyte were insignificantly higher in the ACS group. ACS group had higher total cholesterol and lower high density lipid-cholesterol. However, triglyceride and low density lipid-cholesterol were similar between ACS and control groups. Atherogenic index of plasma (AIP) was significantly higher in ACS group compared to control group (p = 0.029). Similarly, ACS group had higher neutrophil–lymphocyte ratio (NLR) than those in control group. In the subgroups, the NLR were significantly higher in the STEMI group (p < 0.001). However, AIP were similar between the three subgroups (p = 0.748).ConclusionsOur data firstly investigated the lipid-driven inflammatory state in acute coronary syndrome through two easily feasible parameters. There suggest that there are higher AIP and NLR in the ACS patients. Moreover, ACS subgroups are all lipid-driven states, but inflammation levels are different in the entity ACS subgroups.

The relationship between heart rate and mortality of patients with acute coronary syndromes in the coronary intervention era: Meta-analysis.

Background:Most of acute coronary syndromes (ACS) were receiving intervention treatment a high overall rate of coronary angiography in the modern medical practice.Consequently, we conduct a review to determine the heart rate (HR) on the prognosis of ACS in the coronary intervention era. Methods:PubMed, EMBASE, MEDLINE, and the Cochrane Library was systematically searched up to May 2016 using the search terms “heart rate,” “acute coronary syndrome,” “acute myocardial infarction,” “ST elevation myocardial infarction,” “non-ST-segment elevation.” The outcome of interest was all-cause mortality. All analyses were performed using Review Manager. Results:Database searches retrieved 2324 citations. Eleven studies enrolling 156,374 patients were included. In-hospital mortality was significantly higher in the elevated HR group compared to the lower HR group (pooled RR 2.04, 95%CI 1.80–2.30, P < 0.0001). Individuals with elevated admission HR had increased risk of long-term mortality (Pooled RR = 1.63, 95%CI 1.27–2.10, P = 0.008) compared to lower admission HR. The pooled results showed elevated discharge and resting HR were related to increased mortality of patients with ACS (pooled RR 1.88, 95% CI 1.02–3.47, P = 0.04; pooled RR 2.14, 95%CI 1.37–3.33, P < 0.0001, respectively). Conclusion:Elevated HR may increase the mortality of ACS patients in the percutaneous coronary intervention era.

Association of Female Reproductive Factors with Hypertension, Diabetes and LQTc in Chinese Women.

The association of female reproductive factors (FRFs) with cardiovascular risk factors among different population was variable and inconsistent. The objective of this study was to examine the association between FRFs and hypertension, type 2 diabetes mellitus (DM), and long heart-rate-corrected QT interval (LQTc) in Chinese post-menopausal women (Post-MW). A total of 8046 Post-MW from the China Chaoshan Biobank Cohort Study were included for analysis. Logistic regression and general linear regression models were used to estimate the association between FRFs and hypertension, DM, and LQTc. Compared with women with 0 or 1 live birth, increasing risk of hypertension (odds ratio [OR], 1.51; 95% confidence interval [CI], 1.16–1.96), DM (OR, 1.65; 95% CI, 1.22–2.22), and LQTc (OR, 1.45; 95% CI, 1.01–2.09) were observed in women who had five or more live births. Further analysis demonstrated that the association between parity and hypertension, DM, and LQTc was mediated by lifestyle and dyslipidemia. Women with more live births had increased body mass index and waist circumstance, and were inclined to consume more salty food, animal fat, and alcohol, but less meat, vegetable, fish, plant oil, and tea, compared with that had fewer live births (all P < 0.05).