Clinical implications of tenascin-C and OX40 ligand in patients with acute coronary syndrome

Abstract

Abstract. Acute coronary syndrome (ACS) typically occurs when coronary artery disease results in the obstruction of the coronary arteries. Tenascin-C (TNC) and OX40 ligand (OX40L) were shown to be involved in the pathogenesis of atherosclerosis. In this study, 50 healthy controls and 170 patients, including 50 patients with stable angina (SA), 70 with unstable angina and 50 with acute myocardial infarction, were evaluated to assess serum TNC and plasma OX40L levels. The serum TNC levels were measured by a quantitative automated particle-enhanced immunonephelometric assay. ELISA was used to determine the expression levels of OX40L. All the coronary stenoses with a ≥30% diameter reduction were assessed by angiographic coronary stenosis morphology. The patients with ACS exhibited a significant increase in TNC expression levels (39.39±19.80 ng/ml) compared to the levels in the control and SA groups (28.65±12.32 ng̸ml, P<0.01 and 31.22±18.92 ng/ml, P<0.05, respectively). The levels of OX40L were also found to be higher in patients with ACS (38.59±15.76 ng̸ml) compared to those in the control and SA groups (19.42±11.19 ng̸ml, P<0.001 and 21.52±10.30 ng/ml, P<0.001, respectively). The TNC and OX40L levels were positively correlated with each other (r 1 =0.68; P<0.001) and with fibrinogen levels (r 3 =0.76 and r 4 =0.45, respectively; P<0.001). A positive correlation was also observed between the expression of TNC and OX40L and complex coronary stenosis (r 5 =0.69 and r 6 =0.55, respectively; P<0.001). We concluded that TNC and OX40L may act synergistically in coronary plaque formation and may be also be involved in the pathogenesis of coronary lesions. Patients with ACS exhibited increased TNC and OX40L expression levels, which may have created a prothrombotic milieu, aggravating the development of atherosclerosis and the instability of atherosclerotic plaques. Therefore, the expression of TNC and OX40L may be a valuable marker for predicting the severity of ACS.

Value of serum tenascin-C in patients with acute myocardial infarction

“…Recently Yang et al, 19 studied the correlation between serum TN-C and level and angiographically demonstrated complex stenosis in patients with ACS and stable angina from registry of coronary angiography cases. The results of this study demonstrated that the TN-C levels increased as clinical severity increased from Stable Angina to ACS and there was a positive correlation between TN-C expression and the number of complex lesions in patients with ACS.…”

The rs3850641 polymorphism of the TNFSF4 gene increases the risk of myocardial infarction in a Chinese Han population

“…Malarstig et al [ 8 ] suggested that TNFSF4 gene polymorphisms are associated with the incident atherothrombosis and venous thromboembolism risk in Caucasians. Recently, it was also suggested that single nucleotide polymorphisms (SNPs) of the TNFSF4 gene are associated with MI and CHD severity in humans [ 9 ]. Therefore, it is reasonable to hypothesize that the TNFSF4 may be a candidate gene for MI susceptibility.…”

ATF3 Inhibits Tenascin-C-induced Foam Cell Formation in LPS-Stimulated THP-1 Macrophages by Suppressing TLR-4

“…TN-C is an endogenous ligand of toll-like receptor-4 (TLR-4), a key signaling molecule associated with chronic inflammatory conditions 10) , and the levels of both molecules increase in unstable human atheroma 10) . Further, TN-C and OX40 ligand (OX40L) have been shown to be involved in the pathogenesis of atherosclerosis 11) . Altogether, numerous findings have revealed that TN-C may play a role in promoting atherosclerosis, such as its expression at sites of plaque rupture, its involvement in neovascularization, and its ability to influence vascular smooth muscle cell (VSMC) phenotype and pro-inflammatory cytokine/ matrix metalloproteinase (MMP) production 9) .…”