Relationship between functional promoter polymorphism in the XBP1 gene (-116C/G) and atherosclerosis, ischemic stroke and hyperhomocysteinemia

YILMAZ E., Akar R., Eker S., Deda G., Adiguzel Y., Akar N.

MOLECULAR BIOLOGY REPORTS, cilt.37, sa.1, ss.269-272, 2010 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 37 Sayı: 1
  • Basım Tarihi: 2010
  • Doi Numarası: 10.1007/s11033-009-9674-4
  • Dergi Adı: MOLECULAR BIOLOGY REPORTS
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.269-272
  • Anahtar Kelimeler: XBP1 (-116 C/G) polymorphism, Endoplasmic reticulum stress, Atherosclerosis, Stroke, Homocysteinemia, ENDOPLASMIC-RETICULUM STRESS, ER STRESS, FACTOR-V, MUTATION, ROLES
  • Ankara Üniversitesi Adresli: Evet

Özet

ER stress is associated with a range of pathological conditions, among which, the ischemia/reperfusion injury is also found. The mechanistic array of links among the ER stress and thrombovascular diseases is poorly understood. The XBP1 gene is a transcription factor which modulates the ER stress response; and the XBP1 (-116 C/G) gene polymorphism causes an impairment of its positive feedback system. In the present study we investigated the prevalence of XBP1 gene (-116 C/G) polymorphism, separately among the patients with atherosclerosis, ischemic stroke and hyperhomocysteinemia. The G allele and the (-116 G/G) genotype of the XBP1 (-116 C/G) gene polymorphism were found to be a significant risk factor for the patients with Ischemic Stroke. Yet, this allele was seemingly less significant in case of patients with atherosclerosis and hyperhomocysteinemia. Hence, the XBP1 (-116 C/G) gene polymorphism and especially its involvement in a homozygous state are suggested to take active role in the ER stress related ischemia/reperfusion injury.