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. Mater?als 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 p p = 0.0247). Conclus?ons: 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 plaque destabilization, while soluble LIGHT may predominantly functions as a pro-inflammatory cytokine in the inflammatory process.
Highlights
Inflammation has received increasing attention in recent years as a cause of atherosclerosis [1] [2]
Platelet-associated LIGHT may be involved in adhesion of platelets to endothelium, while soluble LIGHT may induce a pro-inflammatory state in vascular endothelial cells via a mechanism that contributes to atherogenesis formation and plaque destabilization as well as an inflammatory process involving leukocyte infiltration into the vessel wall [10] [14]
Our results favor the former notion, since there was a significant correlation between the platelet LIGHT expression levels and Total plaque area (TPA) of carotid artery in the stroke patients
Summary
Inflammation has received increasing attention in recent years as a cause of atherosclerosis [1] [2]. TNF-α and CD40 ligand (CD40L) have been found to have pivotal roles in atherogenesis by eliciting immune responses such as secretion of proinflammatory cytokines, activation of matrix metalloproteinases (MMP) and induction of TF expression [6]-[8] Another TNFSF member, LIGHT (TNFSF14), has recently been reported to demonstrate an enhanced expression in human atherosclerotic plaques and the ability to induce MMP activity in macrophages [9]-[11]. 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. 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
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
