Expression of galectin-3 in human coronary artery and its correlation with plaque structural stability

AIM To investigate the relationship between the expression level of galectin-3 and the stability of plaque structure in human atherosclerotic plaques. METHODS The coronary specimens from autopsy cases （n=84） were collected. Among them, 22 cases had coronary atherosclerotic lesions without sudden death of coronary heart disease （A1 group）, 20 cases were sudden death of coronary heart disease without secondary lesions （A2 group）, 24 cases were sudden death of coronary heart disease with secondary lesions （A3 group）, and 18 cases without heart disease were used as normal control group （control group）. The intimal thickness, necrotic lesion thickness, fibrous cap thickness and the degree of lumen stenosis were measured by routine HE staining in all coronary arteries. The foam cells in the lesion were marked by CD68 and counted. The expression of galectin-3, CD68 and matrix metalloproteinase-2 （MMP-2） in coronary artery intima was detected by immunohistochemical staining, Western blot and RT-qPCR. The correlation between above factors and the structural stability of atherosclerotic plaques was also analyzed. RESULTS Compared with control group, the intima and necrotic lesions were thickened, the fiber cap was thinned, and the degree of lumen stenosis were increased in A1~3 groups （P<0.05）. The number of foam cells in the atherosclerotic focus was increased （P<0.05）. The protein and mRNA levels of galectin-3, CD68 and MMP-2 in the lesions showed an increasing trend from normal group to A1~3 groups （P<0.05）. The expression of galectin-3, CD68 and MMP-2 in atherosclerotic lesions was positively correlated with intimal thickness and necrotic lesion thickness, and negatively correlated with fibrous cap thickness. CONCLUSION The expression of galectin-3 in human coronary atherosclerotic lesions is increased, which is related to the stability of atherosclerotic plaques.