Guosheng Lin

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The aim has been to determine whether the supernatants of mesenchymal stem cells (MSCs) transfected with adenovirus carrying human heme oxygenase-1 (hHO-1) gene protect cardiomyocytes from ischemic injury. We have found that hHO-1 infected MSCs (hHO-1-MSCs) increased expression of hHO-1 protein. Apoptosis of cultured hHO-1-MSCs exposed to hypoxia was(More)
OBJECTIVE Bone marrow mesenchymal stem cells (MSCs) have the potential to repair the infarcted myocardium and improve cardiac function. However, this approach is limited by its poor viability after transplantation, and controversy still exists over the mechanism by which MSCs contribute to the tissue repair. METHODS The human heme oxygenase-1 (hHO-1) was(More)
OBJECTIVES To investigate the protective effect of tumor necrosis factor receptor (TNFR) gene modified mesenchymal stem cells (MSCs) transplantation against inflammation and cardiac dysfunction following acute myocardial infarction (AMI). DESIGN MSCs were extracted from the tibias and femurs of rats and transfected with recombinant adeno-associated viral(More)
BACKGROUND The aim of this study was to investigate the feasibility of an alternative approach to electronic pacemaker by using spontaneously excitable cell grafts as a biological pacemaker in a large animal model of complete atrioventricular block. METHODS AND RESULTS Dissociated male human atrial cardiomyocytes including sinus nodal cells were grafted(More)
BACKGROUND Previous study demonstrated the improvement of cardiac function was proportional to the number of cells implanted. Therefore, increasing cell survival in the infarcted myocardium might contribute to the improvement of the functional benefit of cell transplantation. METHODS AND RESULTS MSCs were treated with IGF-1 in vitro and infused into the(More)
BACKGROUND Sinus node dysfunction and severe heart block are major indications for electronic pacemaker implantation. The aim of the present study was to investigate the feasibility of an alternative approach by using spontaneously excitable cell grafts to serve as a biological pacemaker. METHODS Enzymatically isolated neonatal atrial cardiomyocytes(More)
C3 is common to all pathways of complement activation augmenting ischemia/reperfusion (I/R)-induced myocardial injury and cardiac dysfunction. Complement inhibition with the complement regulatory protein, C1 inhibitor (C1INH), obviously exerts cardioprotective effects. Here, we examine whether C1INH regulates C3 activity in the ischemic myocardial tissue.(More)
Heme oxygenase-1 (HO-1) is a stress-inducible enzyme with diverse cytoprotective effects, and reported to have an important role in angiogenesis recently. Here we investigated whether HO-1 transduced by mesenchymal stem cells (MSCs) can induce angiogenic effects in infarcted myocardium. HO-1 was transfected into cultured MSCs using an adenoviral vector. 1 ×(More)
Acute myocardial infarction (AMI) is associated with inflammation and apoptosis. Emodin plays an anti-inflammatory role in several inflammatory diseases. Recent studies have demonstrated that emodin protects against myocardial ischemia/reperfusion injury. However, its mechanism underlying its effects remains unknown. In a murine model of AMI, based on(More)
Complement activation augments myocardial cell injury and apoptosis during ischemia/reperfusion (I/R), whereas complement system inhibition with C1 inhibitor (C1INH), a serine protease inhibitor, exerts markedly cardioprotective effects. Our recent data demonstrate that C1INH prevents vascular endothelial cell apoptosis and a "modified" form of the reactive(More)
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