Key result
The eNOS T promoter yields ~81% lower transcription efficiency than C, though smoking increases its activity.
Why the study?
The T-786C promoter and 27-bp repeat intron 4 polymorphisms in the eNOS gene have been inconsistently associated with eNOS-related phenotypic changes, motivating exploration of underlying molecular mechanisms.
Population
Preclinical model using pGL3 luciferase reporter vectors and endothelial cell nuclear protein extracts
Comparison
eNOS promoter fragments with T vs C nucleotide at -786 bp and intron 4 with 5x vs 4x27-bp repeats, with or without cigarette smoking extracts
Design
Molecular biology study using reporter vectors and mobility shift assay
Authors
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Preclinical eNOS-smoking interaction data; leaves open human translation to vascular risk stratification.
Absolute Event Rate: 15.7% vs 83.3%
p-value: p=<0.01
The study demonstrates a haplotype-specific expression pattern determined by DNA variants in the eNOS gene that is modifiable by cigarette smoking.
Wang et al. (2002) studied eNOS gene polymorphisms. T promoter at -786 bp vs. C promoter at -786 bp was evaluated on Transcription efficiency (with 5x27-bp enhancer) (p=<0.01). The eNOS T promoter had lower transcription efficiency than the C promoter (15.7% vs 83.3%, P<0.01); cigarette smoking extracts increased T promoter efficiency but reduced C promoter efficiency.
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