Association of chemokines and their receptors genes polymorphisms with risk of myocardial infarction / 中华医学遗传学杂志

<p><b>OBJECTIVE</b>To assess the association of variations in chemokines (CCL5, CCL2), chemokine receptor (CCR5 and CCR2) genes with susceptibility to myocardial infarction (MI) through a case-control study.</p><p><b>METHODS</b>Genotypes of patients with MI (n = 634) were compared with those of controls (n = 601). Genetic polymorphisms of CCL5 rs2107538 (-403G > A), CCL2 rs1024611 (-2518A > G), CCR5 rs333 ( δ 32 ins or del) and CCR2 rs1799864 (190G > A) of 1235 individuals were determined with polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP). Particular genotypes were confirmed with DNA sequencing.</p><p><b>RESULTS</b>No subject was found to carry the CCR5 - δ 32 allele. No association was found between CCL2 rs1024611 and CCR2 rs1799864 polymorphisms and MI. For CCL5 rs2107538 polymorphism, the A allele has occurred at a higher frequency in MI patients than controls, and its AA genotype has been associated with a significantly increased risk of MI independent of conventional risk factors (OR = 3.346, 95%CI = 1.938-5.775, P < 0.01, AA vs. GG). Further analysis indicated that MI patients had significantly more A-403 - A-2518 haplotype (CCL5 -403G > A and CCL2 -2518A > G, 21.8% vs. 26.6%, OR = 1.229, 95%CI = 1.012-1.493, P = 0.038) and AA or AA genotype (CCL5 -403G > A - CCL2 -2518A > G, 5.0% vs. 12.1%, OR = 3.245, 95%CI = 1.780-5.914, P < 0.01).</p><p><b>CONCLUSION</b>Although our data dose not support an association between CCL2 rs1024611, CCR2 rs1799864 and CCR5 rs333 polymorphisms and MI, genetic variation in CCL5 gene may still be a useful marker for assessing susceptibility to MI in ethnic Han Chinese population.</p>

Construction and identification of tetracycline-inducible rat Smad7 eukaryotic expression vector / 南方医科大学学报

<p><b>OBJECTIVE</b>To construct a tetracycline-inducible eukaryotic expression vector of rat Smad7.</p><p><b>METHODS</b>The total RNA was extracted from normal rat kidney with Trizol agent. Rat Smad7 cDNA fragment was cloned by RT-PCR, and was inserted into the restriction site between Nhe I and Hind III of the inducible eukaryotic expression vector pBI-L by tetracycline. pBI-L-Smad7 was constructed by digestion and ligation, and detected by restriction endonuclease digestion and sequencing.</p><p><b>RESULTS</b>The recombinant eukaryotic expression vector pBI-L-Smad7 was constructed correctly as confirmed by restriction endonuclease digestion and sequencing. The fragment of pBI-L-Smad7 digested with restriction endonucleases and the sequence of inserted Smad7 cDNA were consistent with the results of theoretical analysis.</p><p><b>CONCLUSION</b>The tetracycline- inducible eukaryotic expression vector of rat Smad7, pBI-L-Smad7, is constructed successfully, which may facilitate further clinical study of Smad7 gene therapy for tissue and organ fibrosis.</p>

Construction and identification of tetracycline-inducible human hepatocyte growth factor eukaryotic expression vector / 南方医科大学学报

<p><b>OBJECTIVE</b>To construct a tetracycline-inducible eukaryotic expression vector containing human hepatocyte growth factor (HGF) cDNA.</p><p><b>METHODS</b>Human HGF cDNA fragment was obtained by PCR from pUC-SRalpha/HGF plasmid and inserted into the restriction site between Mlu I and Sal I of the tetracycline-inducible eukaryotic expression vector pBI-L. pBI-L-HGF was constructed by DNA recombination in vitro, and was identified by restriction endonucleases digestion and sequencing.</p><p><b>RESULTS</b>The fragment of pBI-L-HGF digested with restriction endonucleases well corresponded to expectation, and the sequence of inserted HGF cDNA was correct according to the GenBank.</p><p><b>CONCLUSION</b>The tetracycline-inducible eukaryotic expression vector of human HGF pBI-L-HGF has been constructed successfully, which allows further study of HGF gene therapy with much safety and easy manipulation.</p>