A Guo1, L Wei, H Shi, X Li, L You. 1. Department of Pathology, General Hospital of PLA, Beijing, 100853 China.
Abstract
OBJECTIVE: To investigate the relationship between matrix metalloproteinase-1 (MMP-1) and coronary atherosclerotic plaque rupture, and the cellular source of MMP-1 within the plaques. METHODS: 42 cases, among which 20 died of acute myocardial infarction, 10 with unstable angina history and 12 with stable angina history but died of other diseases, were selected. All the branch of coronary arteries were examined, parts of the segments were selected for immunohistochemical staining, 5 markers against alpha-smooth muscle actin, CD20, CD45RO, CD68 and MMP-1 were performed. RESULTS: Plaque rupture and thrombosis were found in almost all the cases of acute myocardial infarction and unstable angina. But in the cases of stable angina, the majority of the plaques were stable ones. The expression of MMP-1 in the ruptured plaques were stronger than the unruptured ones (t = -8.07, P < 0.05); Positive relationship was also noted between the expression of CD68 and MMP-1 (r = 0.75, P < 0.05). CONCLUSION: Macrophages are capable of degrading extracellular matrix by secreting MMP-1; Enhanced secretion of MMP-1 within the coronary atherosclerotic plaques has significant relationship with plaque rupture.
OBJECTIVE: To investigate the relationship between matrix metalloproteinase-1 (MMP-1) and coronary atherosclerotic plaque rupture, and the cellular source of MMP-1 within the plaques. METHODS: 42 cases, among which 20 died of acute myocardial infarction, 10 with unstable angina history and 12 with stable angina history but died of other diseases, were selected. All the branch of coronary arteries were examined, parts of the segments were selected for immunohistochemical staining, 5 markers against alpha-smooth muscle actin, CD20, CD45RO, CD68 and MMP-1 were performed. RESULTS: Plaque rupture and thrombosis were found in almost all the cases of acute myocardial infarction and unstable angina. But in the cases of stable angina, the majority of the plaques were stable ones. The expression of MMP-1 in the ruptured plaques were stronger than the unruptured ones (t = -8.07, P < 0.05); Positive relationship was also noted between the expression of CD68 and MMP-1 (r = 0.75, P < 0.05). CONCLUSION: Macrophages are capable of degrading extracellular matrix by secreting MMP-1; Enhanced secretion of MMP-1 within the coronary atherosclerotic plaques has significant relationship with plaque rupture.