Association Between Serum LDL-C and ApoB and SYNTAX Score in Patients With Stable Coronary Artery Disease.

The aim of this study was to examine the relationship between low-density lipoprotein cholesterol (LDL-C) and apolipoprotein (Apo) B levels and the SYNergy between percutaneous coronary intervention with TAXus and cardiac surgery (SYNTAX) score (SS) in patients with stable angina pectoris. We enrolled 594 patients who were suspected to have coronary heart disease (CHD) and who underwent coronary angiography. Patients were divided into 4 groups based on the SS: normal (SS = 0, n = 154), low SS (SS ≤ 22, n = 210), intermediate SS (22 < SS < 32, n = 122), and high SS (SS ≥ 33, n = 63). Positive correlations between lipoprotein (a), LDL-C, ApoB, total cholesterol, and SS were significant ( r = 0.132, 0.632, 0.599, and 0.313, respectively; P < .01), whereas high-density lipoprotein cholesterol (HDL-C), ApoA1, and ApoA1/ApoB levels showed a significant negative correlation ( r = -0.29, -0.344, and -0.561, respectively; P < .01). Multivariate linear regression analysis revealed that LDL-C, ApoB, ApoA1/ApoB, fibrinogen (Fg), and HDL-C levels had an effect on SS (standardized regression coefficients were 0.41, 0.29, -0.12, 0.08, and -0.09, respectively; P < .05). In conclusion, LDL-C, ApoB, ApoA1/ApoB, Fg, and HDL-C levels affected the SS and were predictors of CHD complexity.

Lentiviral vector-mediated co-overexpression of VEGF and Bcl-2 improves mesenchymal stem cell survival and enhances paracrine effects in vitro.

Mesenchymal stem cell (MSC) transplantation has emerged as a promising therapy for ischemic heart disease; however, the low survival rate of transplanted cells limits their therapeutic efficacy. The aim of this study was to investigate whether the dual genetic modification of vascular endothelial growth factor (VEGF) and B­cell lymphoma­2 (Bcl­2) confers a higher expression level of the target genes, better survival and a stronger paracrine effect in MSCs in an adverse environment than the modification of the individual genes. For this purpse, a lentiviral vector was constructed by using a self­cleaving T2A peptide sequence to link and achieve the co­overexpression of VEGF and Bcl­2. Rat MSCs were transfected to obtain cell lines that exhibited a stable overexpression. An in vitro model of oxygen glucose deprivation (OGD) was applied to mimic the ischemic microenvironment, and cell apoptosis, autophagy and the paracrine effects were then determined. Compared with the MSCs in which individual genes were modified and the control MSCs, the MSCs which were subjected to dual genetic modification had a higher expression level of the target genes, a more rapid proliferation, reduced apoptosis, decreased autophagy and an enhanced paracrine effect. Furthermore, the suppression of autophagy was found to contribute to the inhibition of apoptosis in this in vitro OGD model. On the whole, these data indicate that the co­overexpression of VEGF and Bcl­2 protects MSCs in an ischemic environment by inhibiting apoptosis, suppressing autophagy and enhancing the paracrine effects.