miR-155 Regulated Inflammation Response by the SOCS1-STAT3-PDCD4 Axis in Atherogenesis.

Inflammation response plays a critical role in all phases of atherosclerosis (AS). Increased evidence has demonstrated that miR-155 mediates inflammatory mediators in macrophages to promote plaque formation and rupture. However, the precise mechanism of miR-155 remains unclear in AS.

Effect of sex on recovery of ejection fraction in patients with anterior ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention.

Objectives: Myocardial necrosis after ST-segment elevation myocardial infarction (STEMI) can cause left ventricular systolic dysfunction, which has been associated with poor outcomes. Some authors have reported that women have higher mortality rates after primary percutaneous coronary intervention (PCI), but differences between the sexes with regard to recovery of ejection fraction (EF) in patients with STEMI receiving primary PCI have not been evaluated. We aimed to assess the effect of sex on EF recovery in patients with anterior wall STEMI after primary PCI.

Functional blockage of EMMPRIN ameliorates atherosclerosis in apolipoprotein E-deficient mice.

Background: Extracellular matrix metalloproteinase inducer (EMMPRIN), a 58-kDa cell surface glycoprotein, has been identified as a key receptor for transmitting cellular signals mediating metalloproteinase activities, as well as inflammation and oxidative stress. Clinical evidence has revealed that EMMPRIN is expressed in human atherosclerotic plaque; however, the relationship between EMMPRIN and atherosclerosis is unclear. To evaluate the functional role of EMMPRIN in atherosclerosis, we treated apolipoprotein E-deficient (ApoE(-/-)) mice with an EMMPRIN function-blocking antibody.

The effect of the expression of angiotensin II on extracellular matrix metalloproteinase inducer (EMMPRIN) in macrophages is mediated via the AT1/COX-2/PGE2 pathway.

Aim: To explore the expression of extracellular matrix metalloproteinase inducer (EMMPRIN) in THP-1 macrophages induced by angiotensin II (Ang II) and the mechanism of EMMPRIN expression.

Methods: THP-1 cells were cultured and induced into macrophages, then stimulated with 10(-6) mol/L Ang II. Levels of EMMPRIN gene and its protein were measured by real-time polymerase chain reaction and western blotting.

Angiotensin II induces EMMPRIN expression in THP-1 macrophages via the NF-kappaB pathway.

Background: Recent studies on atherosclerosis showed that an inducer of MMPs, EMMPRIN, is highly expressed in human atheromas. This suggested the important role of EMMPRIN in the stability of atherosclerotic plaques. Angiotensin II, one of the main functional peptides in the renin-angiotensin system, is involved in the advancement of atherosclerosis.

Role of TRPC1 and NF-kappaB in mediating angiotensin II-induced Ca2+ entry and endothelial hyperpermeability.

Endothelial dysfunction is associated with cardiovascular diseases. The Ca(2+) influx occurring via activation of plasmalemma Ca(2+) channels was shown to be critical in signaling the increase in endothelial permeability in response to a variety of permeability-increasing mediators. It has been reported that angiotensin II (AngII) could induce Ca(2+) signaling in some cells, and transient receptor potential canonical 1 (TRPC1) had an important role in this process.

[Angiotensin II up-regulates expression of inducible nitric oxide synthase in human umbilical endothelial cells: roles of AT1 and AT2].

Objective: Angiotensin II is an important pro inflammation factor in the cardiovascular system. This experiment is aimed to study the effects of angiotensin II on inducible nitric oxide synthase expression in human umbilical endothelial cells.

Methods: Human umbilical endothelial cells were cultured in vitro and treated with angiotensin II alone or in combination with AT1, AT2 and NF-kappaB inhibitors respectively.

[Tumor necrosis factor alpha and myocardial matrix metalloproteinases in left ventricular remodeling].

Objective: The cytokine tumor necrosis factor (TNF) alpha has been causally linked to left ventricular (LV) remodeling, but the molecular basis for this effect is unknown. It is essential to study the changes of plasma levels of TNF alpha and matrix metalloproteinase-2,3,9 (MMP-2,3,9) expressions in myocardium during congestive heart failure (CHF).

Methods: Plasma levels of TNF alpha were measured with enzyme-linked immunoassay in CHF patients of various degrees and in healthy controls.

[Changes of mitochondrial genes expressed in the brain tissue of rat in stroke-like episodes rats].

Objective: Stroke is a complex disorder caused by a combination of genetic and environmental factors. Epidemiological studies have provided evidence of genetic influence on the development of human stroke. However, genetic changes which contribute to the development of stroke are not well known.

[Change of expression of cell/organs defense genes in brain tissue of rats with stroke-like episodes induced by complex environmental factors].

Objective: To investigate the effect of environmental risk factors on the development of stroke.

Methods: With the use of cold-stimuli plus high-salt intake as environmental risk factors, a hypertension model with the complication of stroke was established in rats, then, a new technique, suppression subtractive hybridization (SSH), was used to identify the differential genes which specifically expressed in total cerebrum tissue of rat in each group. Comparison was made between control group and stroke group.

[Gene expression of Ang II receptors in myocardium in congestive heart failure].

Objective: To explore the relation among myocardial AT(1)-/AT(2)- receptor expression, myocardial remodeling and cardiac function in patients with congestive heart failure.

Methods: Pathologic and morphologic studies on myocardial tissue of 31 patients with CHF due to valvular heart disease and 5 control subjects were carried out with optical and electronic microscopy. Message RNA expression of and AT(1)-/AT(2)-receptors in myocardial tissue were analyzed using the reverse transcriptase-polymerase chain reaction.