title: Associations of VEGF/VEGF-receptor and HGF/c-Met promoter polymorphisms with progression/regression of retinopathy of prematurity.
abstract: OBJECTIVE
  To determine the effect(s) of vascular endothelial growth factor (VEGF), VEGF receptor-2 (VEGFR-2), hepatocyte growth factor (HGF), and HGF receptor (c-Met) polymorphisms on progression/regression of retinopathy of prematurity (ROP) in premature infants.
  
  
  METHODS
  This study comprised both a prospective analysis and a clinically relevant laboratory investigation. Enrolled were 123 Turkish preterm infants--gestational age (GA), ≤34 weeks; birth weight (BW), ≤1500 g--from a single tertiary care center. Infants were grouped as those who had undergone laser therapy (Group 1, n = 42), those with spontaneously regressed ROP (Group 2, n = 50), and those with no ROP (controls) (Group 3, n = 31). VEGF (-634) C and VEGF (-460) C polymorphisms were analyzed using the PCR-restriction fragment length polymorphism (RFLP) (PCR-RFLP) technique. VEGFR-2, HGF, and c-Met gene promoter polymorphisms were determined by direct sequencing.
  
  
  RESULTS
  Mean GAs and BWs of infants in Groups 1 and 2 were statistically significantly lower than those of Group 3 (p = 0.001). Frequencies of VEGF (-634) C and VEGF (-460) C polymorphisms were similar for all groups. We found a +32G→A single-nucleotide polymorphism (SNP) in the promoter region of the VEGFR-2 gene. HGF and c-Met gene promoter polymorphisms were not found in any group.
  
  
  CONCLUSIONS
  Our results indicate that there is no association between the carrier states of gene promoter polymorphisms VEGF (-634) C, VEGF (-460) C, and VEGFR-2, and progression or spontaneous regression of ROP in preterm infants. The absence of HGF and c-Met polymorphisms in our study groups suggests that polymorphisms in the minimal promoters of these genes are not involved in the pathogenesis of ROP.
authors.affiliation: Department of Ophthalmology, Dokuz Eylul University, Izmir, Turkey.
authors.forename: Mahmut
authors.initials: M
authors.lastname: Kaya
authors.forename: Murat
authors.initials: M
authors.lastname: Çokakli
authors.forename: Ayse Tulin
authors.initials: AT
authors.lastname: Berk
authors.forename: Aylin
authors.initials: A
authors.lastname: Yaman
authors.forename: Didem
authors.initials: D
authors.lastname: Yesilirmak
authors.forename: Abdullah
authors.initials: A
authors.lastname: Kumral
authors.forename: Nese
authors.initials: N
authors.lastname: Atabey
mesh_terms: D004247:DNA / Q000235:genetics; D018450:Disease Progression; D005260:Female; D005500:Follow-Up Studies; D005838:Genotype; D005865:Gestational Age; D017228:Hepatocyte Growth Factor / Q000235:genetics* / Q000378:metabolism; D006801:Humans; D007231:Infant, Newborn; D007234:Infant, Premature; D008297:Male; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D011401:Promoter Regions, Genetic; D011446:Prospective Studies; D019859:Proto-Oncogene Proteins c-met / Q000235:genetics* / Q000378:metabolism; D040262:Receptors, Vascular Endothelial Growth Factor / Q000235:genetics* / Q000378:metabolism; D012178:Retinopathy of Prematurity / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D042461:Vascular Endothelial Growth Factor A / Q000235:genetics* / Q000378:metabolism
chemical_list: C066855:HGF protein, human; D042461:Vascular Endothelial Growth Factor A; D017228:Hepatocyte Growth Factor; D004247:DNA; D019859:Proto-Oncogene Proteins c-met; D040262:Receptors, Vascular Endothelial Growth Factor