Abstract
Urotensin II (UII) is involved in the formation of atherosclerosis, but its role in the stability of atherosclerotic plaques is unknown. The purpose of this study was to observe the dynamic changes in plasma UII and analyze its relationship to the stability of atherosclerotic plaques. One hundred thirty-five consecutive patients with acute coronary syndrome (ACS) were enrolled. The plasma UII levels were measured immediately after admission and during three-month follow-up. A vulnerable plaque model was established using local transfection of a recombinant P53 adenovirus into plaques in rabbits fed with a high-cholesterol diet and subjected to balloon arterial injury. The levels of plasma UII were measured weekly. The changes in plasma UII during the formation of atherosclerotic plaques and before and after plaque transfection were observed. The morphology of the plaques and the expression, distribution, and quantitative expression of UII in the plaques also were observed. Our results showed that the levels of plasma UII in patients with ACS at admission were lower than levels observed at the three-month follow-up. UII dynamic changes and its correlation with plaque stabilities were further verified in rabbits with atherosclerotic vulnerable plaques. The UII levels in rabbits were significantly decreased immediately after the P53 gene transfection, which led to plaque instability and rupture. These results suggested that UII expression was down-regulated in ACS, which may be related to its ability to modulate mechanisms involved in plaque stability and instability.
Highlights
The main pathology of coronary heart disease (CHD) is coronary atherosclerosis, characterized by a dynamic change in the stability of atherosclerotic plaques[1]
We have identified that Urotensin II (UII) can be a clinically practicable biomarker of atherosclerotic plaque instability for acute myocardial infarction (AMI)
In AMI patients, the plasma UII level was low at admission and significantly elevated in the post-treatment 3 months follow-up
Summary
The main pathology of coronary heart disease (CHD) is coronary atherosclerosis, characterized by a dynamic change in the stability of atherosclerotic plaques[1]. UII induces monocytes chemotaxis and contributes to the recruitment of monocyte expressing the UT receptor to the atherosclerotic lesions[10]. This event promotes the accumulation of inflammatory cells in the plaque and accelerates foam cells formation[11, 12], which suggests that UII is involved in the development of atherosclerotic plaques. The purpose of this study was to observe the dynamic change of plasma UII and analyze its relationship with the stability of atherosclerotic plaques
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