Investigation of leukocyte RHO/ROCK gene expressions in patients with non-valvular atrial fibrillation

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Duzen I. V., Yavuz F., VURUŞKAN E., Saracoglu E., Poyraz F., Cekici Y., ...Daha Fazla

EXPERIMENTAL AND THERAPEUTIC MEDICINE, cilt.18, sa.4, ss.2777-2782, 2019 (SCI-Expanded) identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 18 Sayı: 4
  • Basım Tarihi: 2019
  • Doi Numarası: 10.3892/etm.2019.7929
  • Dergi Adı: EXPERIMENTAL AND THERAPEUTIC MEDICINE
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED)
  • Sayfa Sayıları: ss.2777-2782
  • Anahtar Kelimeler: atrial fibrillation, gene expression, polymerase chain reaction, Rho proteins, Rho-kinase, RHO-KINASE-ACTIVITY, INHIBITION, ACTIVATION, PROTEINS
  • Ankara Üniversitesi Adresli: Evet

Özet

Atrial fibrillation (AF) is an arrhythmia caused by disorganized electrical activity in the atria, and it is an important cause of mortality and morbidity. There is a limited data about Rho/Rho-kinase (ROCK) pathway contribute to AF development. The aim of the present study was to elucidate leukocyte RHO/ROCK gene expressions in patients with non-valvular AF (NVAF). A total of 37 NVAF patients and 47 age and sex-matched controls were included in this study. mRNA was extracted from leukocytes, and real-time polymerase chain reaction was used for gene expression analysis. A marked increase in ROCK1 and ROCK2 gene expressions in patients with NVAF was observed (P<0.0001). The present study detected significant elevations in RHOBTB2, RND3 (RHOE), RHOC, RHOG, RHOH, RAC3, RHOB, RHOD, RHOV, RHOBTB1, RND2, RND1 and RHOJ gene expressions (P<0.01). However, there were marked decreases in CDC42, RAC2, and RHOQ gene expressions in patients with NVAF. No significant modifications were seen in the other Rho GTPase proteins RHOA, RAC1, RHOF, RHOU and RHOBTB3. To the best of our knowledge, the present study is the first to provide data that gene expression of leukocyte RHO/ROCK may contribute to the NVAF pathogenesis through activated leukocytes, which promotes the immune or inflammatory cascade.