Role of cell adhesion molecules in acute ischemic stroke

Abstract

BACKGROUND AND OBJECTIVES:The expression of soluble adhesion molecules inter-cellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1), besides activation of endothelial cells and transendothelial migration of leukocytes, play an important role in inflammation and progression of ischemic injury after acute stroke. The aim of this study was to determine serum levels of soluble ICAM-1 and VCAM-1 in patients with acute ischemic stroke and controls and correlate them according to etiological subtypes (thromboembolic or lacunar stroke), stroke severity and disability after acute stroke.PATIENTS AND METHODS:Hospital-based prospective study of acute stroke patients hospitalized between December 2008 and September 2009 at the University Hospital Sestre Milosrdnice in Zagreb, Croatia.METHODS:We enrolled 110 patients with acute ischemic stroke and 93 healthy individuals as controls. Serum concentrations of VCAM-1 and ICAM-1 were determined by means of quantitative sandwich enzyme immunoassay. Patients were classified according to etiological subtype, clinical severity of stroke and disability after stroke.RESULTS:There was no significant difference between levels of soluble adhesion molecules VCAM-1 and ICAM-1 in patients and in controls. Levels of VCAM-1 were significantly higher in patients with thromboembolic stroke than in controls. There was no significant correlation between levels of soluble adhesion molecules VCAM-1 and ICAM-1 and stroke severity and disability. There was marked biological interindividual variability in all patient groups.CONCLUSION:This study confirms the role of adhesion molecule VCAM-1 in the pathogenesis of acute thromboembolic stroke.

Dimethyl fumarate confers neuroprotection by casein kinase 2 phosphorylation of Nrf2 in murine intracerebral hemorrhage

“…ICAM-1, which is upregulated after ischemic and hemorrhagic injury, plays an important role in inducing neuro-inflammation and mediating the progression of injury after acute stroke. 5,45 Our results are in line with the work of Thimmulappa et al and Zhao et al who found that activators of the Nrf2/ARE pathway reduced myeloperoxidase, an inflammatory mediator in experimentally induced sepsis, and ICH. 46,47 …”

Blood Markers of Coagulation, Fibrinolysis, Endothelial Dysfunction and Inflammation in Lacunar Stroke versus Non-Lacunar Stroke and Non-Stroke: Systematic Review and Meta-Analysis

“…We included 5 studies [21,27,28,50,51] (344 lacunar strokes) but available data did not permit meta-analysis. In 1 study [21] significantly higher ICAM was found in lacunar stroke versus non-stroke controls acutely; another study [50] found ICAM significantly higher in lacunar versus non-stroke controls chronically.…”

“…Here, 3 studies were included [27,28,51] (121 lacunar strokes) but available data did not permit meta-analysis. Results suggested no difference between lacunar stroke and non-stroke acutely and no difference between lacunar and non-lacunar stroke acutely.…”

Tumor necrosis factor receptor‐associated factor 5 is an essential mediator of ischemic brain infarction

“…; Supanc et al . ). Injured neurons, activated glial cells, and recruited leukocytes secrete cytokine and MMPs that further exacerbate tissue injury (Yang et al .…”

“…Post-ischemic inflammation can aggravate both BBB degradation and neuronal apoptosis (Terao et al 2008;Lakhan et al 2009). Post-ischemic inflammation is initiated through the synthesis of adhesion molecules and chemokines in injured brain cells and is exacerbated by the recruitment of circulating inflammatory cells (Jin et al 2010;Supanc et al 2011). Injured neurons, activated glial cells, and recruited leukocytes secrete cytokine and MMPs that further exacerbate tissue injury Feng et al 2011;del Zoppo et al 2012).…”