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Garlichs, C.D., Kozina, S., Fateh-Moghadam, S., Handschu, R., Tomandl, B., Stumpf, C., Eskafi, S., Raaz, D., Schmeisser, A., Yilmaz, A., Ludwig, J., Neundorfer, B. and Daniel, W.G. (2003) Upregulation of CD40-CD40 Ligand (CD154) in Patients with Acute Cerebral Ischemia. Stroke, 34, 1412-1418.
http://dx.doi.org/10.1161/01.STR.0000074032.64049.47

has been cited by the following article:

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

  AUTHORS: Guangzhi Liu, Yang He, Tingting Yang, Hong Jiang, Yajuan Xiang, Qi Zhang, Xiangjun He, Peter Hjelmstrom, Xuguang Gao

  KEYWORDS: LIGHT, Ischemic Atherosclerotic Stroke, Atherogenesis, Peripheral Blood

  JOURNAL NAME: World Journal of Neuroscience, Vol.4 No.4, August 20, 2014

  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.