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. 2019 Oct;18(4):2777-2782.
doi: 10.3892/etm.2019.7929. Epub 2019 Aug 20.

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

Irfan V Düzen  1 , Fethi Yavuz  2 , Ertan Vuruskan  1 , Erhan Saracoglu  3 , Fatih Poyraz  4 , Yusuf Cekici  3 , Hayri Alıcı  5 , Hüseyin Göksülük  6 , Basar Candemir  6 , Murat Sucu  1 , Abdullah T Demiryürek  7
Affiliations

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

Irfan V Düzen et al. Exp Ther Med. 2019 Oct.

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.

Keywords: Rho proteins; Rho-kinase; atrial fibrillation; gene expression; polymerase chain reaction.

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Figures

Figure 1.
Figure 1.
Comparison of the peripheral blood mRNA ROCK1 and ROCK2 expressions in healthy controls (n=47, solid bars) and in patients with non-valvular atrial fibrillation (NVAF, n=37, open bars). Values are given as mean ± SEM. P<0.0001 and P<0.0001 values were obtained for ROCK1 and ROCK2, respectively. ***P<0.001.
Figure 2.
Figure 2.
Comparison of the peripheral blood mRNA RHOA, RHOBTB2, RND3 (RHOE), RHOC, RHOG, RHOH, RAC3, RHOB, RHOD, RHOV, (A) and RHOBTB1, RND2, RND1, RAC1, RHOJ (B) expressions in healthy controls (n=47, solid bars) and in patients with non-valvular atrial fibrillation (NVAF, n=37, open bars). Values are given as mean ± SEM. P=0.8478, P<0.0001, P<0.0001, P<0.0001, P<0.0001, P<0.0001, P<0.0001, P=0.0003, P<0.0001, P<0.0001, P<0.0001, P<0.0001, P<0.0001, P=0.9273, and P=0.0084 values were obtained for RHOA, RHOBTB2, RND3 (RHOE), RHOC, RHOG, RHOH, RAC3, RHOB, RHOD, RHOV, RHOBTB1, RND2, RND1, RAC1 and RHOJ, respectively. **P<0.01 and ***P<0.001. NVAF, non-valvular atrial fibrillation.
Figure 3.
Figure 3.
Comparison of the peripheral blood mRNA CDC42, RAC2, RHOF, RHOQ, RHOU, and RHOBTB3 expressions in healthy controls (n=47, solid bars) and in patients with non-valvular atrial fibrillation (NVAF, n=37, open bars). Values are given as mean ± SEM, P<0.0001, P<0.0001, P=0.1511, P=0.0060, P=0.7739, and P=0.0511 values were obtained for CDC42, RAC2, RHOF, RHOQ, RHOU, and RHOBTB3, respectively. **P<0.01 and ***P<0.001. NVAF, non-valvular atrial fibrillation.
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