Vascular endothelial growth factor and the risk of smoking-related COPD.

Abstract:

STUDY OBJECTIVES: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), VEGF936*2, has been reported to be associated with significantly lower VEGF plasma levels. Based on these concepts, we hypothesized that VEGF936*1/2 polymorphism may be linked to the development of COPD. DESIGN: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. RESULTS: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. CONCLUSION: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).

journal_name

Chest

journal_title

Chest

authors

Sakao S,Tatsumi K,Hashimoto T,Igari H,Shino Y,Shirasawa H,Kuriyama T

doi

10.1378/chest.124.1.323

subject

Has Abstract

pub_date

2003-07-01 00:00:00

pages

323-7

issue

1

eissn

0012-3692

issn

1931-3543

pii

S0012-3692(15)36027-X

journal_volume

124

pub_type

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