Journal
ASIAN PACIFIC JOURNAL OF TROPICAL MEDICINE
Volume 8, Issue 3, Pages 214-219Publisher
WOLTERS KLUWER MEDKNOW PUBLICATIONS
DOI: 10.1016/S1995-7645(14)60318-7
Keywords
miR-155; Coronary heart disease; RAW264.7 macrophagocyte
Funding
- Shanghai Municipal Key Discipline Construction [ZK2012A27]
- General Program Projects of Pudong Health Bureau of Shanghai [PW2013A-4]
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Objective: To investigate the relationship between the expression level of miR-155 and the severity of coronary lesion, and explore the action mechanism. Methods: Peripheral blood mononuclear cells (PBMC) were isolated form blood simple from patients with acute myocardial infarction (AMI), unstable angina (UAP). stable angina (SAP) and chest pain syndrome (CPS). RT-PCR was performed to analysis the expression level of miR-155 in peripheral blood mononuclear cells, plasma and RAW264.7 macrophagocyte. MTT was used to analyze the cell viability of OxLDL treated RAW264.7 macrophagocyte. Results: The expression level of miR-155 in blood sample from coronary heart disease patients was much lower than in the blood sample of non-coronary heart disease (P<0.05). The level of miR-155 in PBMCs was much higher in the blood sample from CPS group than the other three group, and the level of miR-155 in plasma was higher in the CPS group than in the UAP and the AMI group, the difference was statistically significant (P<0.05). The expression level of miR-155 in PBMCs is positively associated with the level in the plasma (r=0.861, P=0.000). OxLDL can induce the expression of miR-155 in RAW264.7 macrophagocyte, decrease the cell viability of RAW264.7 macrophagocyte, and with the concentration and the treatment time of OxLDL increased, the effort become more obvious. The inhibition effort of OxLDL to RAW264.7 macrophagocyte with high miR-155 expression is much lower than the control group, and it is statistically significant after treated for 12, 24 and 48 h. Conclusions: miR-155 plays a protective role in the progression of atherosclerosis, and it may be achieved by reducing the apoptosis effort of OxLDL to RAW264.7 macrophagocyte.
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