Elevated Plasma Levels but Decreased Platelet-Associated Expression of LIGHT in Patients with Acute Atherothrombotic Stroke

Abstract

Background: As a member of the tumor necrosis factor superfamily (TNFSF), LIGHT (TNFSF14) is expressed by a variety of immune cells and exists in membrane-bound and soluble forms. Recently, LIGHT was found to be associated with platelets and released upon activation. Activation of endothelia cells by recombinant LIGHT protein results in pro-inflammatory and pro-thrombotic changes. Several studies have reported increased plasma levels of LIGHT in patients with stroke and cardiovascular diseases. However, the form-associated roles of LIGHT in ischemic atherosclerotic stroke remain unclear. Materıals and Methods: In this study, the platelet LIGHT expression and soluble LIGHT protein were analyzed by flow cytometry and enzyme-linked immunosorbent assay (ELISA) in peripheral blood of patients with acute ischemic atherosclerotic stroke, asymptomatic carotid stenosis (ACS) and normal controls. RESULTS: During the initial 24 h after onset, the stroke patients had decreased LIGHT expression on their platelets (5.9% ± 4.9%) and increased plasma LIGHT levels (36.1 ± 21.0 pg/ml) as compared with normal controls (9.5% ± 3.0%, p < 0.05; 20.4 ± 13.4 pg/ml, p < 0.05). Moreover, the platelet LIGHT expression correlated with total plaque area in the stroke patients (r = 0.4572, p = 0.0247). Conclusıons: The dysregulated LIGHT expression reflects a persistent chronic inflammatory response that may have been induced during early stages of ischemic atherosclerotic stroke. Our results strongly suggest distinctive roles of form-associated LIGHT in the disease pathogenesis: platelet-associated LIGHT may contribute to formation and development of carotid atherosclerotic plaque, probably involving