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Research on the correlation of TLR4,zinc finger protein A20 in peripheral blood monocyte and tissue factor in acute coronary syndrome patients
Author(s): 
Pages: 63-67+71
Year: Issue:  1
Journal: Journal of Zhenjiang Medical College

Keyword:  acute coronary syndrometoll-like receptor 4zinc finger protein A20tissue factortissue factor passway inhibitor;
Abstract: Objective: To investigate the relation between the expression levels of toll-like 4/A20 mRNA in peripheral blood mononuclear cells( PBMC) and tissue factor,tissue factor passway inhibitor( TFPI) in plasma of patients with acute coronary syndrome( ACS). Methods: The patients of coronary artery diseases( CAD) were divided into the group of ACS( n =31),there were 15 patients with acute myocardial infarction( AMI),and 16 patients with unstable angina pectoris( UAP); and stable angina pectoris( SAP,n = 21) group; the group of control were a total of 20 cases. The expressions of TLR4 and A20 mRNA were detected by real-time fluorescence quantitation polymerase chain reaction( RT-PCR). The concentrations of plasma tissue factor and TFPI were measured by enzyme-linked immunosorbent assay( ELISA). Results: There was a significant correlation between TLR4 mRNA and A20 mRNA in peripheral blood mononuclear cells( r = 0. 640,P = 0. 002). The expressions of A20 and TLR4 mRNA in monocytes in patients with ACS were higher than patients with SAP and healthy persons( P < 0. 001). Comparing with the single lesion group,TLR4 and A20 mRNA positive expression in the multivessel branch lesion group were increased( P =0. 006,P =0. 000). The levels of both tissue factor and TFPI in patients with ACS were significantly higher than the group of SAP and controls( P < 0. 01). Plasma tissue factor was statistically significant between the multivessel disease group and the single lesion group( P = 0. 017). The expression of TLR4 in PBMC group was positively related with the level of TF in ACS( r = 0. 718,P = 0. 000). Conclusion: The increased expression of TLR4 in monocytes was related to atherosclerotic plaque instability as well as coronary artery lesion degree. TLR4-mediated inflammatory pathway activation may promote clotting abnormalities and coronary artery thrombosis in patients with ACS.
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