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Updated: May 23, 2026

A Simple Bioassay for the Evaluation of Vascular Endothelial Growth Factors
Published on: March 15, 2016
Genetic variation in vascular endothelial growth factor-a and lung function.
Angela Simpson1, Adnan Custovic, Robert Tepper
1University of Manchester, Wythenshawe Hospital, Manchester, UK. angela.simpson@manchester.ac.uk
Genetic variations in vascular endothelial growth factor-A (VEGF-A) are linked to lung function across childhood and adulthood. Specific VEGF-A single-nucleotide polymorphisms influence airway function, potentially through alternative splicing.
Area of Science:
- Genetics
- Pulmonology
- Molecular Biology
Background:
- Vascular Endothelial Growth Factor (VEGF) plays a crucial role in lung development.
- Genetic variations within VEGF-A may influence overall lung function.
- Hypothesis: VEGF-A polymorphisms are associated with lung function parameters.
Purpose of the Study:
- To investigate the role of genetic variants in VEGF-A as determinants of airway function.
- To assess lung function from infancy through early adulthood in relation to VEGF-A genotype.
- To replicate findings in pediatric and adult asthma populations.
Main Methods:
- Longitudinal assessment of five VEGF-A single-nucleotide polymorphisms (SNPs) in two birth cohorts.
- Cross-sectional analysis in infants, children, and adults, including those with asthma.
- Functional investigation of the most significant SNP (rs3025028) using Western blotting to quantify VEGF-A isoform ratios.
Main Results:
- Infants with the C-allele of rs3025028 showed significantly higher VmaxFRC and forced expiratory flows.
- This association with improved airway function persisted through preschool, school age, and adolescence.
- Similar findings were observed for FEV1/FVC ratio in adolescents and adults, including those with asthma.
- The ratio of plasma VEGF-A(165b)/panVEGF-A(165) was significantly higher in specific homozygotes.
Conclusions:
- Significant associations were found between VEGF-A SNP rs3025028 and airway function parameters throughout childhood and into adulthood.
- The mechanism may involve altered ratios of active and inhibitory VEGF-A(165) isoforms, potentially regulated by alternative splicing.
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