Phosphorylated proteomics analysis of human coronary artery endothelial cells stimulated by Kawasaki disease patients serum.

Background: Kawasaki disease (KD) is an acute febrile childhood systemic vasculitis that disturbs coronary arteries. The pathogenesis remains unknown. The study of phosphorylated proteins helps to elucidate the relevant pathophysiological mechanisms of cardiovascular disease.

Establishment and characterization of the reversibly immortalized mouse fetal heart progenitors.

Objective: Progenitor cell-based cardiomyocyte regeneration holds great promise of repairing an injured heart. Although cardiomyogenic differentiation has been reported for a variety of progenitor cell types, the biological factors that regulate effective cardiomyogenesis remain largely undefined. Primary cardiomyogenic progenitors (CPs) have a limited life span in culture, hampering the CPs' in vitro and in vivo studies.

[Effect of nesprin-1 in the differentiation of mouse embryonic stem cells into cardiomyocytes].

Objective: To investigate the role of nesprin-1 in mouse embryonic stem cells differentiation into cardiomyocyte.

Methods: Hanging drop-suspension-adherence method was applied for the differentiation of mouse embryonic stem cells into cardiomyocytes under the inducing of salvia miltorrhiza and 5-azacytidine. Changes in nesprin-1 gene expression were detected by using Western blotting and immunofluorescent assay.

[Effect of carvedilol and Radix astragali on ryanodine receptor in heart failure in mice].

Objective: To explore change of ryanodine receptor (RyR) in junior mouse with heart failure (HF) and the effect of β-adrenoreceptor blocker and Radix astragali on RyR in HF in this experiment.

Method: The animal model of congestive heart failure was established by coarctation of abdominal aorta. Five weeks old mice were randomly divided into 4 groups: (1) HF group without treatment (n = 30); (2) HF group treated with carvedilol (n = 30); (3) HF group treated with carvedilol and Radix astragali(n = 30); (4) Sham-operated group (n = 30).

[Preliminary study on the effect of carvedilol on children with primary endocardial fibroelastosis].

Objective: Endocardial fibroelastosis (EFE), a common pediatric cardiovascular disease, often results in chronic heart failure (CHF) and death. Clinical trials have shown that the regimen of combining beta-adrenoreceptor blocker with traditional medicines against CHF can improve left ventricular function and prevent the ventricle from remodeling in patients with CHF. The present study aimed to observe the effect of carvedilol on concentration of plasma brain-type natriuretic peptide (BNP), and safety in children with EFE.

[Expression of connective tissue growth factor in cardiomyocyte of young rats with heart failure and benazepril intervention].

Objectives: Ventricular remodeling is an important pathologic progress in almost all end stage heart failure (HF), and it is characterized by ventricular thickening and cardiac fibrosis with poor prognosis. The connective tissue growth factor (CTGF), a new growth factor with multi-function, has an important role in fibrosis of tissue and organs. It has been demonstrated that angiotensin-converting enzyme inhibitor (ACEI) can prevent the development of cardiomyocyte from remodeling and improve cardiac function.

[Effect of carvedilol on ryanodine receptor in heart failure].

Objective: The release of intracellular stores of Ca(2+) occurs virtually in all types of cells by a means of amplifying external signals that modulate intracellular signaling events. In cardiac myocytes, type 2 ryanodine receptor (RyR(2)) is activated during excitation-contraction (E-C) coupling by Ca(2+)-induced Ca(2+) release (CICR) triggered by Ca(2+) influx across the sarcolemma. The hyperadrenergic state of heart failure results in leaky RyR(2) channels attributable to PKA hyperphosphorylation and depletion of the stabilizing FK506 binding protein, FKBP12.