Background Mesenchymal stem cells (MSCs) transplantation provides a new approach for myocardial repair. However, many important fundamental questions about MSCs transplantation remain unanswered. There is an urgent need to identify MSCs from the beating heart and analyze the efficacy of this new approach. This study aimed to localize the magnetically labeled MSCs (MR-MSCs) and monitor the restorative effects of MR-MSCs with magnetic resonance (MR) imaging. Methods Acute myocardial infarction (AMI) was created in swine by a balloon occlusion of the left anterior descending coronary artery. Cells were delivered via intracoronary infusion after myocardial infarction. Infarct size change and cardiac function were assessed with 3.0T MR scanner. The results were then confirmed by histological and western blot analysis. All statistical procedures were performed with Systat (SPSS version 12.01). Results A total of 26 swine were divided into four groups (sham-operated group, n=6; AMI group with PBS transplantation, n=6; labeled MSCs group, n=7; unlabeled MSCs group, n=7). MSCs, MR-MSCs (107cells) or PBS were delivered by intracoronary injection after MI and serial cardiac MR imaging studies were performed at 0, 4 and 8 weeks after transplantation. MR imaging demonstrated MI size decreased after MSCs transplantation in labeled and unlabeled groups, however, increases were seen in the AMI group at 8 weeks after MI. The left ventricular ejection fraction (LVEF) was slightly increased in the AMI group ((41.87±2.45)% vs (39.04±2.80)%, P＞0.05), but significantly improved in the MR-MSCs group ((56.85±1.29)% vs (40.67±2.00)%, P＜0.05) and unlabeled group ((55.38±1.07)% vs (41.78±2.08)%, P＜0.05) at 8 weeks after treatment. MR-MSCs were further confirmed by Prussian blue and immunofluorescent staining. Western blot analysis demonstrated that there was an increased expression of cardiomyocyte markers such as myosin heavy chain and troponin T in the MSCs treatment groups and the ratio of matrix metalloproteinase 2 to tissue inhibitor of metalloproteinase 1 decreased in the labeled group and unlabeled group compared with the AMI group and sham-operated group. Conclusion Transplanted MR-MSCs can regenerate new myocardium and prevent remolding in an MI model at 2-month follow-up and represent a preferred method to better understand the mechanisms of stem cell therapy in future clinical studies.

Toll-like receptors (TLRs) play roles in innate and adaptive immune responses. Some TLRs are involved in the pathogenesis of cardiovascular diseases. Coronary artery disease (CAD) has an inflammatory and immunological basis. We investigated whether TLR8 Met1Val and TLR8-129G＞C single nucleotide polymorphisms (SNPs rs3764879 and rs3764880) are associated with CAD in the Chinese population. We enrolled 412 consecutive patients (185 with coronary stenosis ≥50% or previous myocardial infarction and 227 controls). Ligase detection reaction was performed to detect SNPs rs3764879 and rs3764880 of TLR8. The SNP at rs3764879 is in complete linkage disequilibrium with rs3764880. No significant difference was found in genotypic or allelic frequencies of these two common SNPs between CAD cases and controls (P＞0.05, respectively). No associations existed between these two SNPs and the severity of coronary artery stenosis (All P＞0.05). These results do not support an involvement of SNPs rs3764879 and rs3764880 of TLR8 in predisposition to CAD.

Objective: Tetramethylpyrazine, a drug originally isolated from the rhizome of Ligusticum walliichi, is an inhibitor of phosphodiesterase and inhibits platelet aggregation and smooth muscle cell proliferation. The effect of the tetramethylpyrazine-eluting stent (TES) on preventing in-stent restenosis was investigated in comparison with control bare metal stents in a porcine coronary stent restenosis model. Methods: The TES was prepared by spray-coating the 2.5 to 3.0mm×15 to 20mm bare metal stents with Tetramethylpyrazine monomer, methyl methacrylate copolymer, and polyglycolic acid. Stent overdilation injury (stent:artery=1.1 to 1.2:1.0) was made with control bare stents (n=5) and TES (n=5) in porcine coronary arteries. Follow-up quantitative coronary angiography (QCA) and histopathological assessments of stented coronary arteries were performed 4 weeks after stenting. Results: Quantitative coronary angiography showed the late lumen loss (0.28±0.08mm versus 1.70±0.52mm; P=0.004) and percentage diameter stenosis (10.0±2.1% versus 60.2±23.5%; P=0.01) were significantly lower in the TES group than that in the control group. Histopathological assessments of stented coronary arteries showed that the injury score and the in-stent area were similar between the groups (P＞0.05), whereas the lumen area was significantly larger (4.34±0.93 mm2 versus 1.29±1.02mm2; P=0.011) in the TES group than that in the control group. The number of proliferating cell nuclear antigen-positive cells was also significantly decreased in the TES group compared with the control group (14.7±2.5% versus 23.6±3.2%; P=0.008). Moreover, apoptosis was enhanced in TES group while regrowth of endothelium was similar between the groups. Conclusions: TES inhibited the neointimal hyperplasia and reduced in-stent restenosis in a porcine coronary artery restenosis model.

Background We examined the -2518G/A polymorphism of the MCP-1 gene, its plasma levels, and premature stableCADin a Chinese population. Methods The study comprised 132 patients with premature stable CAD (cases) and 153 controls. Genotypes were determined by ligase detection reaction-polymerase chain reaction sequencing and grouping. Plasma MCP-1 level was detected with enzyme-linked immunosorbent assay. Results No differences were found between genotype distribution and allele frequencies of MCP-1 gene -2518 G/A polymorphism (AA:18.1%; AG:51.5%; GG:30.3% in cases; AA:16.3%; AG:52.9%; GG:30.7% in controls; P=0.918). The G allele prevalence was 0.561 in cases and 0.572 in controls (P=0.786). No significant difference was found in plasma MCP-1 level between cases and controls [(47.50±26.65) vs. (41.05±15.71)pg/ml, P=0.272)] or among the 3 genotypes [AA, (43.49±10.50) pg/ml; AG, (46.09±25.08)pg/ml; GG, (40.03±18.13)pg/ml; P=0.381]. Logistic regression analysis confirmed the lack of association between MCP-1-2518 G/A single nucleotide polymorphism and premature stable CAD after adjustment for confounding parameters. Conclusions The MCP-1-2518 G/A single nucleotide polymorphism does not affect plasma levels of MCP-1 or susceptibility to premature stableCADin a Chinese population.