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

Düzen,Irfan   V.; Yavuz,Fethi; Vuruskan,Ertan; Saracoglu,Erhan; Poyraz,Fatih; Cekici,Yusuf; Alıcı,Hayri; Göksülük,Hüseyin; Candemir,Basar; Sucu,Murat; Demiryürek,Abdullah   T.

doi:10.3892/etm.2019.7929

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

Authors:
- Irfan V. Düzen
- Fethi Yavuz
- Ertan Vuruskan
- Erhan Saracoglu
- Fatih Poyraz
- Yusuf Cekici
- Hayri Alıcı
- Hüseyin Göksülük
- Basar Candemir
- Murat Sucu
- Abdullah T. Demiryürek
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Affiliations: Department of Cardiology, Faculty of Medicine, University of Gaziantep, Gaziantep 27310, Turkey, Department of Cardiology, Adana City Hospital, Adana 01060, Turkey, Department of Cardiology, Dr Ersin Arslan Education and Research Hospital, Gaziantep 27310, Turkey, Department of Cardiology, Defa Life Hospital, Gaziantep 27310, Turkey, Department of Cardiology, Hatem Hospital, Gaziantep 27310, Turkey, Department of Cardiology, Faculty of Medicine, Ankara University, Ankara 06340, Turkey, Department of Medical Pharmacology, Faculty of Medicine, University of Gaziantep, Gaziantep 27310, Turkey
Published online on: August 20, 2019 https://doi.org/10.3892/etm.2019.7929
Pages: 2777-2782
Copyright: © Düzen et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

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.

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