Endothelial microparticle levels are similar in acute ischemic stroke and stroke mimics due to activation and not apoptosis/necrosis.

BACKGROUND Endothelial microparticles (EMPs) are <2-microm membranous blebs from endothelial cell membranes that have been demonstrated to be elevated in vasculopathic conditions. One study has demonstrated elevated EMPs in acute ischemic stroke (AIS) versus age- and comorbidity-matched controls. OBJECTIVES To determine the level of EMPs in stroke mimics and AIS and determine if EMPs are released as a result of activation or apoptosis/necrosis in AIS. METHODS EMP levels in plasma of patients with AIS and stroke mimic patients were quantified by flow cytometry. Stroke status was verified in all patients by magnetic resonance imaging. Patients were matched for age and comorbidities. Markers for apoptosis/necrosis (platelet/endothelial cell adhesion molecule-1 [PECAM-1]/CD31 antigen) and activation (E-selectin/CD62e antigen) were compared. A PECAM-1/E-selectin ratio of >4.0 was used to determine whether EMPs were generated via activation or apoptosis/necrosis. Data were compared between groups using the Mann-Whitney U test. RESULTS EMP levels were similar in stroke mimic patients when compared with AIS; there was no difference between groups (PECAM-1, p = 0.393; E-selectin, p = 0.579). The PECAM-1/E-selectin ratio was also similar for AIS and stroke mimics, and all were >4.0. CONCLUSIONS EMP levels were similar in patients with AIS and stroke mimic patients. The PECAM-1/E-selectin ratio demonstrated that EMPs were generated via activation and not apoptosis/necrosis. This suggests that EMPs may not be a good marker for AIS, given the inability to discriminate between stroke mimics and AIS.

[1]  J. Broderick,et al.  Association of Serial Biochemical Markers With Acute Ischemic Stroke: The National Institute of Neurological Disorders and Stroke Recombinant Tissue Plasminogen Activator Stroke Study , 2006, Stroke.

[2]  B. Loriod,et al.  Thrombin-induced endothelial microparticle generation: identification of a novel pathway involving ROCK-II activation by caspase-2. , 2006, Blood.

[3]  A. Baird,et al.  Circulating endothelial microparticles in acute ischemic stroke: a link to severity, lesion volume and outcome , 2006, Journal of thrombosis and haemostasis : JTH.

[4]  S. Virani,et al.  Postprandial Hypertriglyceridemia Increases Circulating Levels of Endothelial Cell Microparticles , 2004, Circulation.

[5]  L. Horstman,et al.  Endothelial microparticles correlate with high-risk angiographic lesions in acute coronary syndromes , 2004 .

[6]  N. Young,et al.  Elevated circulating endothelial membrane microparticles in paroxysmal nocturnal haemoglobinuria , 2004, British journal of haematology.

[7]  L. Horstman,et al.  Endothelial microparticles as markers of endothelial dysfunction. , 2004, Frontiers in bioscience : a journal and virtual library.

[8]  T. Back,et al.  The natural course of lesion development in brain ischemia. , 2004, Acta neurochirurgica. Supplement.

[9]  R. Nieuwland,et al.  Antigenic characterization of endothelial cell‐derived microparticles and their detection ex vivo , 2003, Journal of thrombosis and haemostasis : JTH.

[10]  L. Horstman,et al.  High levels of circulating endothelial microparticles in patients with acute coronary syndromes. , 2003, American heart journal.

[11]  L. Horstman,et al.  Endothelial cells release phenotypically and quantitatively distinct microparticles in activation and apoptosis. , 2003, Thrombosis research.

[12]  Richard A. Preston,et al.  Effects of Severe Hypertension on Endothelial and Platelet Microparticles , 2003, Hypertension.

[13]  Patrice Darmon,et al.  Type 1 and type 2 diabetic patients display different patterns of cellular microparticles. , 2002, Diabetes.

[14]  K. Egashira Clinical importance of endothelial function in arteriosclerosis and ischemic heart disease. , 2002, Circulation journal : official journal of the Japanese Circulation Society.

[15]  W. Jy,et al.  Agonist-induced capping of adhesion proteins and microparticle shedding in cultures of human renal microvascular endothelial cells. , 2002, Endothelium : journal of endothelial cell research.

[16]  A. Tedgui,et al.  Circulating Microparticles From Patients With Myocardial Infarction Cause Endothelial Dysfunction , 2001, Circulation.

[17]  A. Tedgui,et al.  Current perspective on the role of apoptosis in atherothrombotic disease. , 2001, Circulation research.

[18]  J. Freyssinet,et al.  Elevated levels of shed membrane microparticles with procoagulant potential in the peripheral circulating blood of patients with acute coronary syndromes. , 2000, Circulation.

[19]  B. Björkerud,et al.  Apoptosis is abundant in human atherosclerotic lesions, especially in inflammatory cells (macrophages and T cells), and may contribute to the accumulation of gruel and plaque instability. , 1996, The American journal of pathology.

[20]  M. Petri,et al.  Surface blebs on apoptotic cells are sites of enhanced procoagulant activity: implications for coagulation events and antigenic spread in systemic lupus erythematosus. , 1996, Proceedings of the National Academy of Sciences of the United States of America.