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Updated: Aug 29, 2025
A Simple Bioassay for the Evaluation of Vascular Endothelial Growth Factors
Published on: March 15, 2016
Molecular Polymorphisms of Vascular Endothelial Growth Factor Gene and Bronchopulmonary Dysplasia in Very Low Birth
Laura Filonzi1, Serafina Perrone2, Maria Luisa Tataranno3
1Department of Chemistry, Life Sciences and Environmental Sustainability, University of Parma, Italy.
Insights
Genetic variations in VEGF and VEGFR1 are not linked to bronchopulmonary dysplasia (BPD) in very low birth weight infants. Further research is needed to identify genetic factors contributing to BPD development.
Area of Science:
- Neonatal Medicine
- Genetics
- Pulmonology
Background:
- Bronchopulmonary dysplasia (BPD) is a significant chronic lung disease in preterm infants.
- Despite advances, BPD remains a costly complication, influenced by prematurity, ventilation, oxidative stress, and inflammation.
- Gene polymorphisms regulating angiogenesis and alveolarization are potential contributors to BPD risk.
Purpose of the Study:
- To investigate the association between vascular endothelial growth factor (VEGF) gene polymorphisms and the development of BPD in very low birth weight (VLBW) newborns.
Main Methods:
- Study included 82 VLBW infants (33 with BPD, 49 controls).
- Two polymorphisms, VEGFR1-710 C/T and VEGF +936 C/T, were analyzed from saliva samples.
- Genomic DNA was extracted and purified using a standard kit.
Main Results:
- Significant differences observed between BPD and control groups in gestational age, birth weight, ventilation, oxygen therapy duration, and maternal conditions (preeclampsia, chorioamnionitis).
- No statistically significant differences were found in genotypic or allelic levels for the studied VEGFR1 and VEGF polymorphisms between the groups.
Conclusions:
- The investigated single nucleotide polymorphisms in VEGF and VEGFR1 genes are not associated with BPD onset in VLBW infants.
- Further research is required to identify specific gene polymorphisms involved in vascular development that contribute to BPD.
Background:
Bronchopulmonary dysplasia (BPD) is a chronic lung disease affecting primarily preterm and very low birth weight (VLBW) infants. Despite the advances in perinatal care, BPD remains a major clinical and costly complication in premature infants. The pathogenesis of BPD is complex and multifactorial. Prematurity, mechanical ventilation, oxidative stress, and inflammation are recognized as major interrelated contributing factors. Recently, some candidate genes involved in angiogenesis and alveolarization regulating mechanisms have been associated to BPD risk development. The aim of this study was to evaluate the role of vascular endothelial growth factor (VEGF) polymorphisms on BPD onset in VLBW newborns.
Methods:
Eighty-two VLBW infants, without major anomalies, were consecutively enrolled: 33 developed BPD (BPD group) and 49 infants without BPD served as controls (control group). In all infants, two polymorphisms, respectively (VEGF receptor) VEGFR1-710 C/T and VEGF +936 C/T, were determined through salivary brush. Genomic DNA was extracted and purified from saliva samples by using the MasterAmp Buccal Swab DNA Extraction Kit (Tebu-bio, Milan, Italy).
Results:
Significant statistic differences were found between BPD newborns and controls with regard to gestational age, birth weight, mechanical ventilation, duration of oxygen therapy, maternal preeclampsia, and chorioamnionitis. No differences were detected between genotypic and allelic levels regarding VEGFR1 and VEGF molecular polymorphisms.
Conclusions:
Two single nucleotide polymorphisms within VEGF and VEGFR1 genes are not associated with BPD. Further researches are needed to reveal gene polymorphisms involved in vascular development as contributors to the onset of BPD.
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