Ascending aortic constriction in rats for creation of pressure overload cardiac hypertrophy model.

Ascending aortic constriction is the most common and successful surgical model for creating pressure overload induced cardiac hypertrophy and heart failure. Here, we describe a detailed surgical procedure for creating pressure overload and cardiac hypertrophy in rats by constriction of the ascending aorta using a small metallic clip. After anesthesia, the trachea is intubated by inserting a cannula through a half way incision made between two cartilage rings of trachea.

Quercetin attenuates Monocyte Chemoattractant Protein-1 gene expression in glucose primed aortic endothelial cells through NF-kappaB and AP-1.

Monocyte Chemoattractant Protein-1 (MCP-1) is involved in the diapedesis of blood monocytes into the arterial intima, an early critical event in atherogenesis. Modulating MCP-1 expression can be a key strategy to decrease the risk for atherosclerosis in diabetes. We hypothesized that quercetin, an anti-inflammatory molecule could modulate high glucose concentration (HG) induced MCP-1 expression in aortic endothelial cells in vitro because of its regulatory effects on Activator Protein-1 (AP-1) and Nuclear Factor-kappaB (NF-kappaB).

Effects of epidermal growth factor on proliferation and migration of cardiosphere-derived cells expanded from adult human heart.

Recent studies have provided evidence that the human heart has an endogenous reserve of cardiac stem cells (CSCs) that can be activated to reconstitute the dead myocardium. Current efforts are now directed towards the identification of factors favoring the growth and expansion of the CSC pool in the heart. Accordingly, in the present study, effects of different growth factors on cardiosphere-derived cells (CDCs), expanded from atrial biopsies from patients undergoing elective coronary artery bypass surgery, were analyzed.

Curcumin attenuates glucose-induced monocyte chemoattractant protein-1 synthesis in aortic endothelial cells by modulating the nuclear factor-kappaB pathway.

Background/aims: High glucose (HG) induces monocyte chemoattractant protein-1 (MCP-1) synthesis in endothelial cells through nuclear factor kappaB (NFkappaB). We investigated whether curcumin, losartan and sodium salicylate (NaSal) attenuate HG-induced MCP-1 synthesis in rat aortic endothelial cells (RAECs) and explored the mechanism of action.

Methods: RAECs were stimulated with HG (25 mmol/l) for 24 h in the presence or absence of curcumin, losartan, NaSal or NFkappaB inhibitor, Bay 11-0782.

Genetic engineering with endothelial nitric oxide synthase improves functional properties of endothelial progenitor cells from patients with coronary artery disease: an in vitro study.

Recent studies have reported a marked impairment in the number and functions of endothelial progenitor cells (EPCs) in patients with coronary artery disease (CAD). In view of an important role of eNOS in angiogenesis, in the present study, we evaluated the effects of eNOS gene transfer in ex vivo expanded EPCs isolated from patients with CAD. The expanded EPCs were transfected with mammalian expression vector pcDNA3.

Endocardial endothelial cells stimulate proliferation and collagen synthesis of cardiac fibroblasts.

Given that vascular endothelial cells play an important role in the modulation of vascular structure and function, we hypothesized that endocardial endothelial cells (EECs) may have a modulator role in regulating the cardiac interstitial cells. Endocardial endothelial cells were isolated from freshly collected pig hearts and cardiac fibroblasts were isolated from 3- to 4-d-old Wistar rats. Fibroblasts were cultured in the presence or absence of conditioned medium from EECs.

Immortalization and characterization of porcine ventricular endocardial endothelial cells.

Endocardial endothelial cells (EECs), which form the inner lining of the cavities of the heart, are a distinct cell population whose dysfunction can be critical in pathological conditions of heart. Insights into the role and organization of these cells in pathological states of the heart are limited mainly due to a dearth of experimental models. To date no endocardial endothelial cell line is available.

Cerium depresses endocardial endothelial cell-mediated proliferation of cardiac fibroblasts.

Cerium has been implicated in the pathogenesis of cardiac disorders such as acute myocardial infarction and endomyocardial fibrosis (EMF). A geochemical hypothesis for the causation of EMF linked the cardiac lesions to magnesium deficiency consequent to malnutrition and increased cardiac levels of cerium derived from monazite soils in the coastal regions of the tropics. We tested the hypothesis that the stimulus for fibroblast proliferation and enhanced collagen synthesis in EMF is derived from cardiac endothelial cells activated or injured by cerium.

Molecular mechanisms in endothelial regulation of cardiac function.

Endothelium is now recognized as a massive, regionally specific, multifunctional organ. Given its strategic anatomic location between the circulating blood components and the vascular smooth muscle or the cardiac muscle, it is a biologically significant interface whose dysfunction can be a critical factor in various pathological conditions. Two types of endothelial cells are recognized in the heart, the endocardial endothelial (EE) cells and the microvascular endothelial cells (MVE).