AIM To investigate the role of long non-coding RNA MRGPRF-6:1 (lnc-MRGPRF-6:1) in macrophages lipid metabolism in atherosclerosis.
METHODS The expression of lnc-MRGPRF-6:1 in plasma of control group (n=20) and coronary artery disease (CAD) patients (n=20) was measured by reverse transcription polymerase chain reaction (qRT-PCR). Commercial kits were used to detect The content of total cholesterol (TC) and triglyceride (TG) were detected in all patients and control group and the correlation between lnc-MRGPRF-6:1 and TC and TG was analyzed. Subsequently, we constructed lnc-MRGPRF-6:1 knockdown macrophages and control group macrophages respectively. The content of TC, TG, malondialdehyde (MDA) and reactive oxygen species (ROS) and the activity of superoxide dismutase (SOD) in macrophages were measured by commercial kits. Cell viability was detected by CCK-8 and cell apoptosis was analyzed by flow cytometry.
RESULTS The expression of lnc-MRGPRF-6:1 and the content of TC and TG in the plasma of CAD patients were significantly increased (P<0.05) and the expression of lnc-MRGPRF-6:1 was positively correlated with the content of TC and TG. After the knockdown of lnc-MRGPRF-6:1, the lipid accumulation of macrophages decreased significantly. Meanwhile, the content of TC, TG, MDA and ROS was significantly decreased (P<0.05), the activity of SOD increased remarkably (P<0.05), the cell viability was improved extremely (P<0.05) and cell apoptosis was decreased in the lnc-MRGPRF-6:1 knockdown macrophages.
CONCLUSION lnc-MRGPRF-6:1 accelerates lipid accumulation and lipid peroxidation in macrophages of atherosclerosis.