Sakao Seiichiro, Tatsumi Koichiro, Hashimoto Tomohiro, Igari Hidetoshi, Shino Yuji, Shirasawa Hiroshi, Kuriyama Takayuki
Department of Respirology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Chest. 2003 Jul;124(1):323-7. doi: 10.1378/chest.124.1.323.
Vascular endothelial growth factor (VEGF) signaling may be required for maintenance of the alveolar structures, and alveolar septal cell apoptosis could contribute to the pathogenesis of COPD presenting emphysematous changes; however, the common mutation at position 936 in the 3' untranslated region of the VEGF gene, a C to T substitution (the C allele was denoted as 1, and the T allele as 2), VEGF9362, has been reported to be associated with significantly lower VEGF plasma levels. Based on these concepts, we hypothesized that VEGF9361/2 polymorphism may be linked to the development of COPD.
The differences in VEGF936*1/2 allele frequency were examined in 113 patients with smoking-related COPD and two control groups (101 smoker/ex-smoker control subjects and 102 population control subjects) using the polymerase chain reaction-restriction fragment length polymorphism technique.
VEGF936*1/2 allele frequencies did not differ among the groups: 0.792/0.208 in COPD patients, 0.822/0.178 in smoker/ex-smoker control subjects, and 0.842/0.152 in population control subjects.
The 936 C/T polymorphism of the VEGF gene (including both homozygous and heterozygous) was not associated with the development of COPD (odds ratio, 1.23; 95% confidence interval, 0.760 to 1.995).
