VEGF, sVEGFR-1 and Endostatin Serum Levels and VEGF Polymorphisms in Recurrent Aphthous Stomatitis


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YÜCE S., BAĞCI B., BAĞCI G., DOĞAN M., Koc S., SEZGİN İ., ...Daha Fazla

JOURNAL OF CLINICAL AND ANALYTICAL MEDICINE, cilt.7, sa.5, ss.701-705, 2016 (ESCI) identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 7 Sayı: 5
  • Basım Tarihi: 2016
  • Doi Numarası: 10.4328/jcam.4523
  • Dergi Adı: JOURNAL OF CLINICAL AND ANALYTICAL MEDICINE
  • Derginin Tarandığı İndeksler: Emerging Sources Citation Index (ESCI), Scopus, TR DİZİN (ULAKBİM)
  • Sayfa Sayıları: ss.701-705
  • Sivas Cumhuriyet Üniversitesi Adresli: Evet

Özet

Aim: Recurrent aphthous stomatitis (RAS) is one of the most frequent diseases of the oral mucosa, characterized by chronic, painful, recurrent, and necrotizing ulcerations. The precise etiology and pathogenesis of RAS have not been clarified. Therefore. we aimed to investigate serum levels of VEGF. sVEGFR-1, and endostatin as well as the frequencies of VEGF +936 C/T and -1154 C/A single nucleotide polymorphisms (SNPs) in Turkish patients with recurrent aphthous stomatitis. Material and Method: Forty-two patients with RAS (24 minor RAS and 18 major RAS) and 37 healthy subjects were included in the study. Serum levels of VEGF, sVEC FR-1, and endostatin were measured using the ELISA method. VEGF +936 C/T and-1154 C/A SNPs were determined by the PCR-RFLP method. Results: The mean serum level of VEGF was found higher in bearing CC genotype of +936 CFI SNP compared with CT genotype (639.5 +/- 309.1 vs 442.1 +/- 197.8: p = 0.032). VEGF-1154 GA genotype was found to be more frequent in patients with minor RAS and GG genotype was more frequent in patients with major RAS (p = 0.022). There was a significant difference between minor RAS and major RAS with regard to mean VEGF serum levels (677.1 +/- 316.7 vs 492.9 +/- 242.7; p = 0.032). Discussion: The T allele of +936 C/T SNP is associated with decreased serum VEGF level, and this decrease may have a contributory role in impaired neovascularization and re-epithelialization in the etiology and pathogenesis of RAS. Further studies are needed to determine the role of VEGF in RAS susceptibility and its clinical manifestations.