Association between TNFSF4 tagSNPs and myocardial infarction in a Chinese Han population.

Tumor necrosis factor superfamily member 4 (TNFSF4) plays an important role in atherosclerosis development. However, the biological significance of TNFSF4 variants on myocardial infarction (MI) pathogenesis remains poorly understood. We investigated the influence of 5 TNFSF4 tagging single nucleotide polymorphisms (rs3861950, rs17346501, rs7518045, rs1234313, and rs3850641) on individual susceptibility to MI in a Chinese population of 285 MI patients and 645 controls. Genotyping was performed using the polymerase chain reaction-ligase detection reaction method. In multivariate logistic regression analysis, only the TNFSF4 tagging single nucleotide polymorphism rs7518045 exhibited a significant effect on MI risk; A allele (odds ratio = 0.68, 95% confidence interval = 0.46-1.00, P = 0.048) and AA genotype (odds ratio = 0.64, 95% confidence interval = 0.42-0.97, P = 0.036) were associated with a decreased risk of MI compared with the G allele and the combined AG/GG genotype, respectively. Moreover, the haplotype rs3861950C-rs17346501C-rs7518045A-rs1234313G containing the rs7518045 A allele also exhibited a significant association with a decreased risk for MI (odds ratio = 0.42, 95% confidence interval = 0.21-0.84, P = 0.011). Our study showed that the A allele of the rs7518045 and haplotype rs3861950C-rs17346501C-rs7518045A-rs1234313G in the TNFSF4 gene were associated with decreased MI risk in a Chinese Han population. Further studies using larger sample sizes and in diverse ethnic populations are needed to confirm the general validity of our findings.

Deletion of the lmna gene induces growth delay and serum biochemical changes in C57BL/6 mice.

The A-type lamin deficient mouse line (Lmna (-/-) ) has become one of the most frequently used models for providing insights into many different aspects of A-type lamin function. To elucidate the function of Lmna in the growth and metabolism of mice, tissue growth and blood biochemistry were monitored in Lmna-deficient mice, heterozygous (Lmna (+/-) ) and wide-type (Lmna (+) (/) (+) ) backcrossed to C57BL/6 background. At 4 weeks after birth, the weight of various organs of the Lmna (-/-), Lmna (+/-) and Lmna (+) (/) (+) mice was measured. A panel of biochemical analyses consisting of 15 serological tests was examined. The results showed that Lmna deficient mice had significantly decreased body weight and increased the ratio of organ to body weight in most of tissues. Compared with Lmna (+) (/) (+) and Lmna (+/-) mice, Lmna (-/-) mice exhibited lower levels of ALP (alkaline phosphatase), Chol (cholesterol), CR (creatinine), GLU (glucose), HDL (high-density lipoprotein cholesterol) and higher levels of ALT (alanine aminotransferase) (p<0.05). Lmna (-/-) mice displayed higher AST (aspartate aminotransferase) values and lower LDL (lowdensity lipoprotein cholesterol), CK-MB (creatine kinase-MB) levels than Lmna (+) (/) (+) mice (p<0.05). There were no significant differences among the three groups of mice with respect to BUN (blood urea nitrogen), CK (creatine kinase), Cyc C (cystatin C), TP (total protein), TG (triacylglycerols) and UA (uric acid) levels (p>0.05). These changes of serological parameters may provide an experimental basis for the elucidation of Lmna gene functions.