Background: Morbidities related to atherosclerosis, such as acute coronary syndrome (ACS), remain the leading cause of mortality. Axl is a receptor tyrosine kinase that is expressed in mammalian vascular and immune cells. Axl signaling is involved in the regulation of the inflammatory response. A considerable amount of evidence indicates that inflammation is responsible for the development of atherosclerosis in patients with ACS.
Methods: To assess the relation of Axl and ACS, we recruited 64 patients with coronary heart disease: 34 with ACS, 30 with stable coronary heart disease, and 24 apparently healthy controls. Serum concentrations of soluble Axl (sAxl) were quantified by enzyme-linked immunosorbent assay. High-sensitivity C-reactive protein, tumor necrosis factor alpha, troponin I, and other routine biochemical markers were also measured.
Results: The levels of sAxl were significantly higher in patients with ACS than in the controls (P=0.005). Furthermore, correlation analysis indicated that sAxl was significantly associated with serum levels of high-sensitivity C-reactive protein (r=0.283, P=0.008), tumor necrosis factor alpha (r=0.565, P<0.001), and troponin I (r=0.264, P=0.013). Logistic regression analysis (odds ratio=1.038, 95% confidence interval, 1.008-1.069, P=0.012) indicated a significant association between sAxl and ACS.
Conclusions: Serum levels of sAxl correlate to inflammatory biochemical markers. These findings demonstrate for the first time that sAxl does have a role in ACS, presumably connected to the inflammation.