Neuropilin 1 ameliorates electrical remodeling at infarct border zones in rats after myocardial infarction.

Background: Electrical remodeling at infarct border zone (IBZ) has been shown to contribute to the occurrence of ventricular arrhythmias after myocardial infarction (MI). Sema3A has been demonstrated to reduce the inducibility of ventricular arrhythmias. Neuropilin 1 (NRP1) is the receptor of Sema3A.

Slit3 regulates migration of endothelial progenitor cells by activation of the RhoA/Rho kinase pathway.

Nerves and blood vessels are in close proximity, indicating possible biomolecular interactions. Slit/Robo signaling pathways play critical roles in cell proliferation and motility. Endothelial progenitor cells (EPCs) participate in angiogenesis and vascular homeostasis.

Urotensin II promotes the proliferation of endothelial progenitor cells through p38 and p44/42 MAPK activation.

Urotensin II (UII) is a vasoactive peptide with many potent effects in the cardiorenovascular system and is also possibly involved in the pathogenesis of atherosclerosis. Endothelial progenitor cells (EPCs) are involved in angiogenesis and vascular homeostasis and may be important in the maintenance of endothelial integrity. The aim of this study was to investigate whether UII has an effect on the proliferation of bone marrow-derived EPCs and the possible signaling mechanisms involved.

Semaphorin 3A attenuates electrical remodeling at infarct border zones in rats after myocardial infarction.

Electrical remodeling at infarct border zone has been shown to contribute to the occurrence of ventricular arrhythmias after myocardial infarction (MI). Electrical remodeling is causally associated with sympathetic neural remodeling in MI. Semaphorin 3A (Sema3A), a potent neural chemorepellent for sympathetic axons, has been demonstrated to suppress sympathetic neural remodeling after MI.

Down-regulation of CREB-binding protein expression inhibits thrombin-induced proliferation of endothelial cells: possible relevance to PDGF-B.

Thrombin acts as a potent mitogenic factor for ECs (endothelial cells) by the release of several growth factors, including PDGF-B (platelet-derived growth factor-B). CBP (CREB-binding protein), which functions as a transcriptional coactivator, links the changes in the extracellular stimuli with alterations in gene expression. Therefore, we hypothesized that CBP could mediate thrombin-induced proliferation of ECs via PDGF-B-dependent way.

Minocycline protects against myocardial ischemia and reperfusion injury by inhibiting high mobility group box 1 protein in rats.

Minocycline has been shown to protect against myocardial ischemia and reperfusion injury. However, the mechanism remains unclear. This study was to investigate the role of high mobility group box 1 protein (HMGB1) in the cardioprotection of minocycline during myocardial ischemia and reperfusion in rats.

Carvedilol ameliorates sympathetic nerve sprouting and electrical remodeling after myocardial infarction in rats.

Background: We hypothesized that carvedilol, a nonselective β-blocker, can exert antiarrhythmogenic effects by inhibiting sympathetic nerve sprouting and electrical remodeling at peri-infarct zones after myocardial infarction (MI).

Methods: MI was induced by ligation of the coronary artery. The rats in the carvedilol group received 5.

Pretreatment with B-type natriuretic peptide protects the heart from ischemia-reperfusion injury by inhibiting myocardial apoptosis.

The therapy for acute myocardial infarction (AMI) has been improved; yet, AMI remains a major cause of death and heart failure in industrialized countries. B-type natriuretic peptide (BNP), a hormone secreted from the heart, has been shown cardioprotective effects during myocardial ischemia/reperfusion. In the present study, we aimed to examine whether BNP could inhibit myocardial apoptosis during ischemia/reperfusion.

Increased serum HMGB1 is related to the severity of coronary artery stenosis.

Background: High mobility group box 1 (HMGB1) protein has been identified as a novel pro-inflammatory cytokine in coronary artery disease (CAD). We investigated the relationship between serum HMGB1 level and the severity of coronary artery stenosis.

Methods: Serum HMGB1 concentration in patients was measured by ELISA.

Carvedilol ameliorates the decreases in connexin 43 and ventricular fibrillation threshold in rats with myocardial infarction.

Connexin 43 (Cx43) is the most prominent connexin in the mammalian ventricular myocardium and forms gap junctions that are essential for normal conduction of action potential. Carvedilol, a nonselective beta-blocker, is widely used to prevent ventricular arrhythmias after myocardial infarction (MI). Here, we examined the effect of carvedilol on the expression of Cx43 protein and ventricular fibrillation threshold (VFT) using a rat MI model.

[Effects of sympathetic nerve stimulation on connexin43 and ventricular arrhythmias during acute myocardial ischemia: experiment with rats].

Objective: To investigate the effects of sympathetic nerve stimulation (SNS) on connexin43 (Cx43) and ventricular arrhythmias during acute myocardial ischemia (MI).

Methods: Ninety five Wistar rats were randomly divided into four groups: MI group (n=25), undergoing: ligation of the anterior descending coronary; MII-SNS group (n=25); undergoing electric stimulation of sympathetic nerve since the beginning of ligation of the anterior descending coronary and lasting till 30 min after the ligation, sympathetic nerve stimulation preconditioning + myocardial ischemia (pSNS-MI) group (n=25), undergoing electric stimulation of sympathetic nerve since the beginning of ligation of the anterior descending coronary that ended just after the ligation; and sham operation (SO) group (n=20), without coronary ligation. Ventricular arrhythmias were monitored by electrocardiography.

Effects of sympathetic nerve stimulation on ischemia-induced ventricular arrhythmias by modulating connexin43 in rats.

Background: Increased cardiac sympathetic nerve activity is thought to contribute to ventricular tachyarrhythmias during acute myocardial ischemia (MI). However, the mechanism is not completely understood. This study investigated the effects of sympathetic nerve stimulation (SNS) on ventricular tachyarrhythmias and connexin43 (Cx43) during acute MI in rats.

Dysregulation of CREB binding protein triggers thrombin-induced proliferation of vascular smooth muscle cells.

Thrombin is a potent mitogen for vascular smooth muscle cells (VSMCs). CBP has been regarded as a potential therapeutic target on the basis of its ability to affect cell growth. Therefore we hypothesized that CBP mediates thrombin-induced proliferation of VSMCs.

[Intra-arterial transfusion of endothelial progenitor cells accelerate reendothelialization in balloon-denuded rabbit carotid arteries].

Objective: To investigate the effects of endothelial progenitor cells (EPCs) transfusion on reendothelialization and neointima proliferation in balloon-denuded rabbit carotid arteries.

Method: Bone marrow-derived rabbit mononuclear cells (MNCs) were cultured in endothelial basal medium to form EPCs. The cell makers were assayed by immunocytochemistry.