Agonist-induced Piezo1 activation promote mitochondrial-dependent apoptosis in vascular smooth muscle cells.

Objective: Mechanical damage plays an essential role in the progression of atherosclerosis. Piezo1 is a new mechanically sensitive ion channel. The present study investigated the vascular smooth muscle cells (VSMCs) apoptosis induced by Piezo1 activation and explored its underlying mechanism.

Nε-carboxymethyl-lysine-induced PI3K/Akt signaling inhibition promotes foam cell apoptosis and atherosclerosis progression.

Advanced glycation end products (AGEs) are closely associated with diabetic macrovascular complications. The present study aimed to investigate the effects of Nε-Carboxymethyl-Lysine (the key active component of AGEs) in diabetic atherosclerosis on foam cell apoptosis and to explore the underlying mechanisms. Tissue sections were collected from 12 Type 2 diabetic patients and 4 control patients who underwent amputation surgery following a car accident.

Dynamic Ghrelin and GH serum levels during combined simultaneous arginine clonidine stimulation test in children with dwarfism.

Background: Combined simultaneous arginine clonidine stimulation (CSACS) test represents a more appropriate stimulus to detect Ghrelin, for it does not affect glucose metabolism.

Methods: Fifty prepubertal children with dwarfism were recruited and further classified into normal growth hormone (NGH) and growth hormone deficiency (GHD) group with growth hormone (GH) peak cut-off value of 10 μg/l. In both groups, GH and Ghrelin serum levels were determined after the GH provocation test at 30, 60, and 120 min and the height standard deviation score (SDS) for bone age was measured six months later.

Cardiac resynchronization therapy for heart failure induced by left bundle branch block after transcatheter closure of ventricular septal defect.

A 54-year-old female patient with congenital heart disease had a persistent complete left bundle branch block three months after closure by an Amplatzer ventricular septal defect occluder. Nine months later, the patient suffered from chest distress, palpitation, and sweating at daily activities, and her 6-min walk distance decreased significantly (155 m). Her echocardiography showed increased left ventricular end-diastolic diameter with left ventricular ejection fraction of 37%.

Bisoprolol reverses epinephrine-mediated inhibition of cell emigration through increases in the expression of β-arrestin 2 and CCR7 and PI3K phosphorylation, in dendritic cells loaded with cholesterol.

The effect of bisoprolol on dendritic cell (DC) migration was investigated, including the analysis of protein expression, cytokine secretion and activation of the PI3K-pathway. The chemotactic cell numbers in cholesterol-loaded DCs treated with epinephrine were significantly decreased by 26.66±6.

The relationship between CD40 gene polymorphism and unstable coronary atherosclerotic plaques.

Background: Recently, CD40 polymorphism was found to be associated with acute coronary syndromes. However, few study was involved in the relationship between CD40 polymorphism and the risk of the vulnerable plaque to rupture so far.

Materials And Methods: A total of 699 patients who have received coronary angiography were divided into 3 groups according to the morphological division of the plaques: complex lesions (343 cases), smooth lesions (131 cases), and control group (225 cases).

Association analysis of CD40 gene polymorphism with acute coronary syndrome.

Current evidence shows that the CD40-CD40 ligand (CD40-CD40L) system plays a crucial role in the development, progression and outcome of acute coronary syndrome (ACS). The aim of this study is to investigate whether a CD40 gene (-1C/T) single nucleotide polymorphism (SNP) is associated with ACS and CD40 expression. We included controls (n = 163) and patients with either ACS (n = 210) or stable angina (SA, n = 189) in the study.

Upregulation of OX40-OX40 ligand system on T lymphocytes in patients with acute coronary syndromes.

Objective: To investigate whether upregulation of OX40-OX40 ligand (OX40L) system is related to stability of coronary atherosclerotic plaque in patients with coronary heart diseases.

Methods: Thirty normal controls and 250 patients, including 80 with stable angina (SA), 110 with unstable angina (UA), and 60 with acute myocardial infarction (AMI), were enrolled in our study. The expression of OX40 and OX40L in peripheral CD4 T lymphocytes were analyzed by flow cytometry.

OX40-OX40 ligand interaction may activate phospholipase C signal transduction pathway in human umbilical vein endothelial cells.

Studies have recently supported the emerging role of OX40/OX40L interaction in atherosclerosis. The mechanism of OX40/OX40L interaction may be related to a variety of signal pathways. The most important signal pathway involves the activation of phospholipase C (PLC) which induces diacylglycerol-protein kinase C (DAG-PKC) and the inositol trisphosphate (IP(3))-intracellular free calcium ([Ca(2+)](i)) pathway.

The clinical implications of increased OX40 ligand expression in patients with acute coronary syndrome.

Background: Increasing evidence show that OX40 ligand (OX40L), also known as tumor necrosis factor superfamily member 4 (TNFSF4), plays an important role in the pathogenesis of atherosclerosis. We investigated whether expression levels of soluble OX40L in serum and of membrane OX40L on platelets were related to serum concentrations of matrix metalloproteinases (MMPs) and stability of coronary atherosclerotic plaque in patients with acute coronary syndrome (ACS).

Methods: We included healthy controls (n=30), patients with stable angina (SA) (n=40) and patients with ACS, including unstable angina (UA) (n=70) and acute myocardial infarction (AMI) (n=40).

Relationship between CD40 ligand expression and B type natriuretic peptide levels in patients with chronic heart failure.

Background: Inflammation plays a pathogenic role in the development of chronic heart failure (CHF). Increasing evidence shows that CD40-CD40 ligand (CD40L) interaction plays a pathogenic role in inflammatory disorders. We assessed whether CD40 ligand expression was abnormal in patients with CHF.

Losartan inhibited expression of matrix metalloproteinases in rat atherosclerotic lesions and angiotensin II-stimulated macrophages.

Aim: To explore whether the angiotensin II (Ang II) receptor 1 (AT1) antagonist, losartan could reduce activity and expression of matrix metalloproteinases (MMPs) in rat atherosclerotic plaques.

Methods: Male Wistar-Kyoto rats were ip injected a single dose of vitamin D3 600 kU x kg(-1) x month(-1) and fed an atherogenic diet for 4 months to induce experimental atheroma. Then either placebo or losartan 50 mg x kg(-1) x d(-1) was administered in rats for another 2 months.