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Influences of matrix metalloproteinase-3 gene variation on extent of coronary atherosclerosis and risk of myocardial infarction

Seyyare Beyzade, BSc^*, Shaoli Zhang, PhD^*, Yuk-ki Wong, MD, MRCP, Ian N. M. Day, MB, PhD, FRCPath^*, Per Eriksson, PhD and Shu Ye, MD, PhD^*,*

^* Human Genetics Division, Southampton University Medical School, Southampton, United Kingdom
Cardiothoracic Unit, Southampton General Hospital, Southampton, United Kingdom
Atherosclerosis Research Unit, Karolinska Hospital, Stockholm, Sweden

View larger version (12K): [in a new window]   Figure 1 Schematic presentation of all polymorphisms identified in the matrix metalloproteinase-3 gene.

View larger version (56K): [in a new window]   Figure 2 Results of electrophoretic mobility shift assays. Two double-stranded oligonucleotide probes corresponding to the T and C alleles, respectively, of the –1986 T>C polymorphism were labeled with 32P and incubated with nuclear extracts from macrophages (U937 [a] and MonoMac-6 [b]), followed by polyacrylamide gel electrophoresis and autoradiography. The arrow indicates a DNA–protein complex that is more readily detectable with the T probe (lanes 2 and 5) than the C probe (lanes 4 and 9). The DNA–protein complex is readily competed with unlabeled T probe (lanes 6 and 10), weakly competed with unlabeled C probe (lanes 7 and 11), but not affected by a nonspecific competitor (lanes 8 and 12).