TY - JOUR
T1 - 4G/5G promoter polymorphism of plasminogen activator inhibitor-1, lipid profiles, and ischemic stroke
AU - Chen, Chih-Hung
AU - Eng, Hock Liew
AU - Chang, Chih-Jen
AU - Tsai, Tzu-tung
AU - Lai, Ming Liang
AU - Chen, Hsiao Yen
AU - Liu, Chien Ju
AU - Lin, Tsun Mei
PY - 2003/8/1
Y1 - 2003/8/1
N2 - The 4G allele of common 4G/5G polymorphism in the promoter of the plasminogen activator inhibitor-1 (PAI-1) gene is associated with increased PAI-1 transcription and has been proposed as a candidate genetic risk factor for thrombotic diseases. We investigated the relationship between this polymorphism and lipid profiles and stroke risk. One hundred patients with ischemic stroke and 150 age- and sex-matched control subjects were enrolled. PAI-1 genotype was determined with the use of polymerase chain reaction and restriction-length analysis. Genotype distribution in the stroke group was 40% 4G/4G, 46% 4G/5G, and 14% 5G/5G; in the control group it was 38.7% 4G/4G, 45.3% 4G/5G, and 16% 5G/5G. The allele and genotype frequencies of 4G/5G polymorphism were not different between the stroke and control groups. Control subjects who were homozygous for the 4G allele had significantly lower high-density lipoprotein (HDL) cholesterol levels than did those carrying the 5G allele (51. 2 ± 11.8 vs 58.4 ± 15.8 mg/dL; P = .002). In the control group, regression analysis revealed a significant contribution of 4G/4G genotype to increased triglyceride (P = .042) and to decreased HDL cholesterol (P < .001) levels. Our findings suggest that PAI-1 4G/5G promoter polymorphism alone is not associated with ischemic stroke. However, this polymorphism influences lipid levels, and the underlying mechanism must be determined.
AB - The 4G allele of common 4G/5G polymorphism in the promoter of the plasminogen activator inhibitor-1 (PAI-1) gene is associated with increased PAI-1 transcription and has been proposed as a candidate genetic risk factor for thrombotic diseases. We investigated the relationship between this polymorphism and lipid profiles and stroke risk. One hundred patients with ischemic stroke and 150 age- and sex-matched control subjects were enrolled. PAI-1 genotype was determined with the use of polymerase chain reaction and restriction-length analysis. Genotype distribution in the stroke group was 40% 4G/4G, 46% 4G/5G, and 14% 5G/5G; in the control group it was 38.7% 4G/4G, 45.3% 4G/5G, and 16% 5G/5G. The allele and genotype frequencies of 4G/5G polymorphism were not different between the stroke and control groups. Control subjects who were homozygous for the 4G allele had significantly lower high-density lipoprotein (HDL) cholesterol levels than did those carrying the 5G allele (51. 2 ± 11.8 vs 58.4 ± 15.8 mg/dL; P = .002). In the control group, regression analysis revealed a significant contribution of 4G/4G genotype to increased triglyceride (P = .042) and to decreased HDL cholesterol (P < .001) levels. Our findings suggest that PAI-1 4G/5G promoter polymorphism alone is not associated with ischemic stroke. However, this polymorphism influences lipid levels, and the underlying mechanism must be determined.
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U2 - 10.1016/S0022-2143(03)00063-5
DO - 10.1016/S0022-2143(03)00063-5
M3 - Article
C2 - 12960956
AN - SCOPUS:0141630329
VL - 142
SP - 100
EP - 105
JO - Translational Research
JF - Translational Research
SN - 1931-5244
IS - 2
ER -