Fractalkine receptor polymorphism may not be associated with the development and clinical course of ulcerative colitis

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Gokcan H., Yurtcu E., Selcuk H., Sahin F. I.

BOSNIAN JOURNAL OF BASIC MEDICAL SCIENCES, cilt.15, sa.2, ss.73-77, 2015 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 15 Sayı: 2
  • Basım Tarihi: 2015
  • Doi Numarası: 10.17305/bjbms.2015.387
  • Dergi Adı: BOSNIAN JOURNAL OF BASIC MEDICAL SCIENCES
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.73-77
  • Anahtar Kelimeler: Fractalkine, CX3CR1 polymorphism, ulcerative colitis, INFLAMMATORY-BOWEL-DISEASE, EVIDENCE-BASED CONSENSUS, CROHNS-DISEASE, INTRAEPITHELIAL LYMPHOCYTES, CHEMOKINE FRACTALKINE, RECRUITMENT, CX(3)CR1, GENE, IDENTIFICATION, MIGRATION
  • Ankara Üniversitesi Adresli: Hayır

Özet

Fractalkine (CX3C), a chemokine expressed by epithelial cells within normal and inflamed colorectal mucosa, induces leukocyte adhesion and migration via fractalkine receptor. The aim of this study was to investigate two single nucleotide polymorphisms of the fractalkine receptor gene as a risk factor both for the development and clinical findings of ulcerative colitis. In this study, si patients with ulcerative colitis (UC) and 8o controls were recruited. Genotypes of fractalkine receptorc.743G>A (V249I) and c.839C>T (T280M) polymorphisms were identified by restriction fragment length polymorphism analyses after polymerase chain reaction.Genotype distribution and allele frequencies of V249I and T280M were not statistically significantly different between UC and control groups (p>0.05). No statistically significant relationship was found between fractalkine receptor polymorphisms and clinical findings of UC. We observed no significant difference in fractalldne receptor polymorphism between patients and control group and no genotype-phenotype relation. Therefore, we concluded that fractalkine receptor polymorphisms may not contribute to the molecular pathogenesis of UC.