Open AccessModulation of TNF-α plasma levels in coronary artery disease [CAD] and non-CAD male patients by lncRNA UCA1 and aspirin
Author(s) -
Peyman Nowrouzi-Sohrabi,
Atefeh Seghatoleslam,
Peyman Izadpanah,
Mehran Erfani,
Hassan Ahmadvand,
Mehdi Kalani
Publication year - 2020
Publication title -
archives of biological sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.217
H-Index - 25
eISSN - 1821-4339
pISSN - 0354-4664
DOI - 10.2298/abs200616040n
Subject(s) - coronary artery disease , aspirin , peripheral blood mononuclear cell , tumor necrosis factor alpha , medicine , downregulation and upregulation , interleukin 6 , cad , immunology , cytokine , biology , gene , in vitro , biochemistry
The aim of this study was to investigate the expression of long non-coding RNA urothelial carcinoma-associated 1 (UCA1) and its role in TNF-? production as one of the main inflammatory cytokines, in peripheral blood mononuclear cells (PBMCs) of patients with coronary artery disease (CAD) and healthy non-CAD (NCAD) individuals as the control group. Fifteen CAD and 15 NCAD individuals were enrolled in the study. UCA1 expression in PBMCs and the plasma concentrations of interleukin (IL)-6, IL-22 and tumor necrosis factor (TNF)-? were assessed by real-time PCR and flowcytometry, respectively. UCA1 expression was not significantly different between the CAD and NCAD groups, however, its level was higher in PBMCs of regular aspirin users of both study groups. Furthermore, aspirin users showed a significantly lower plasma level of TNF-? in comparison to non-aspirin users. In addition, UCA1 expression was negatively correlated with the level of TNF-? in the total sample of the examined population. It seems that the increased levels of UCA1 may be an underlying mechanism for downregulation of TNF-? in aspirin users.