Abstract
Bronchopulmonary dysplasia (BPD) is a chronic lung disease that mainly affects premature newborns. Many different factors, increasingly genetic, are involved in the pathogenesis of BPD. The aim of the study is to investigate the possible influence of fibronectin SNP on the occurrence of BPD. The study included 108 infants born between 24 and 32 weeks of gestation. BPD was diagnosed based on the National Institutes of Health Consensus definition. The 5 FN1 gene polymorphisms assessed in the study were the following: rs3796123; rs1968510; rs10202709; rs6725958; and rs35343655. BPD developed in 30 (27.8%) out of the 108 preterm infants. Incidence of BPD was higher in infants with lower APGAR scores and low birthweight. Investigation did not confirm any significant prevalence for BPD development in any genotypes and alleles of FN1. Further studies should be performed to confirm the role of genetic factors in etiology and pathogenesis of BPD.
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The datasets generated during and analyzed during the current study are available from the corresponding author on reasonable request.
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KK and DS designed research; KK, KG, AS, DS, JAA, SRA, and LMK collected and analyzed the data; KK, DS, JAA, AS, SRA, LMK, MS-B, KD, AS-M, and GK performed research; GK was responsible for PCR procedure. All authors commented on the manuscript at all grades.
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Kosik, K., Sowińska, A., Seremak-Mrozikiewicz, A. et al. Polymorphisms of fibronectin-1 (rs3796123; rs1968510; rs10202709; rs6725958; and rs35343655) are not associated with bronchopulmonary dysplasia in preterm infants. Mol Cell Biochem 477, 1645–1652 (2022). https://doi.org/10.1007/s11010-022-04397-1
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DOI: https://doi.org/10.1007/s11010-022-04397-1