Plasma Membrane-Derived Vesicles in Sickle Cell Disease: A Possible Indicator of the Continuous Endothelial Stimulation and/or Injury to Blood Cells
American Journal of Biomedical and Life Sciences
Volume 1, Issue 4, December 2013, Pages: 99-102
Received: Dec. 19, 2013; Published: Dec. 30, 2013
Views 2967      Downloads 168
Authors
Samuel Antwi-Baffour, Department of Medical Laboratory Sciences, School of Allied Health Sciences, College of Health Sciences, University of Ghana, P. O. Box KB 143, Korle-Bu, Accra, Ghana
Abena Nyarkoah Wiredu, The Central Laboratory, Korle-bu Teaching Hospital, Accra, Ghana
Ransford Kyeremeh, Department of Medical Laboratory Sciences, School of Allied Health Sciences, College of Health Sciences, University of Ghana, P. O. Box KB 143, Korle-Bu, Accra, Ghana
Seidu Abdulai Mahmood, Department of Medical Laboratory Sciences, School of Allied Health Sciences, College of Health Sciences, University of Ghana, P. O. Box KB 143, Korle-Bu, Accra, Ghana
Article Tools
PDF
Follow on us
Abstract
Plasma membrane-derived vesicles (PMVs) are released into circulation in response to normal and stress/pathogenic conditions. They are of tremendous significance for the prediction, diagnosis, and observation of the therapeutic success of many diseases. Knowledge of their functional properties would contribute to a better understanding of the pathological mechanisms leading to various diseases in which their levels are raised. The objective of this study was to quantify and compare the levels of PMVs in sickle cell disease patients (Hb SS and Hb SC) with non-sickle cell (Hb AA) subjects. The comparison will help us research and understand the processes that lead to their constitutive release in sickle cell disease patients than in their normal counterparts. A total of one hundred and fifty (150) sickle cell disease patients (study group) and blood donors (control group) that consented to partake in the study were recruited. There were 82 males and 68 females. Fifty (50) each of Hb SS, Hb SC and Hb AA samples were obtained. Sodium metabisulphite (sickling) test, Haemoglobin electrophoresis and quantification of PMVs were carried out on all the samples. The sickle cell disease patients had elevated levels; SS (38.89 ± 0.73 × 104/ml; p= 0.01) and SC (32.62 ± 1.18 × 104/ml; p = 0.01) as against the control subjects (Hb AA) who had average PMVs of 11.28 ± 0.29 × 104/ml PFP (mean ± SEM). It was concluded that both SS and SC (study) samples showed an increased count of PMVs as compared to the AA (control) samples, suggesting persistent endothelial stimulation and/or injury of blood cells leading to continuous shedding of PMVs in sickle cell disease patients.
Keywords
PMVs, Sickle Cell Disease, Electrophoresis, Flow Cytometer
To cite this article
Samuel Antwi-Baffour, Abena Nyarkoah Wiredu, Ransford Kyeremeh, Seidu Abdulai Mahmood, Plasma Membrane-Derived Vesicles in Sickle Cell Disease: A Possible Indicator of the Continuous Endothelial Stimulation and/or Injury to Blood Cells, American Journal of Biomedical and Life Sciences. Vol. 1, No. 4, 2013, pp. 99-102. doi: 10.11648/j.ajbls.20130104.14
References
[1]
Perumbeti A, Malik P (2010). Genetic correction of sickle cell anemia and β-thalassemia: progress and new perspective. The Scientific World Journal 10: 644–654.
[2]
Kato GJ, Hebbel RP, Steinberg MH, Gladwin MT (2009). Vasculopathy in sickle cell disease: Biology, pathophysiology, genetics, translational medicine, and new research directions. Am J Haematol 84(9): 618-625.
[3]
Lionnet F, Hammoudi N, KS Stojanovic1, AvellinoV, Grateau G, Girot R and Haymann JP (2012). Hemoglobin SC disease complications: a clinical study of 179 cases. Haematol 97(8): 1136-1141.
[4]
Ballas SK, Lieff S, Benjamin LJ, Dampier CD, Heeney MM, Hoppe C, Johnson CS, Rogers ZR, Smith-Whitley K, Wang WC, Telen MJ (2010). Definitions of the phenotypic manifestations of sickle cell disease. Am J Haematol 85(1): 6-13.
[5]
Morel O, Hugel B, Jesel L, Zobairi F, Bareiss P, Freyssinet JM, Toti F (2004). Procoagulant membranous microparticles and atherothrombotic complications in diabetics. Arch Mal Coeur Vaiss 97(10): 1006-1012.
[6]
Boulanger CM, Scoazec A, Ebrahimian T, Henry P, Mathieu E, Tedgui A, Mallat Z (2001). Circulating microparticles from patients with myocardial infarction cause endothelial dysfunction. Circulation 104(22): 2649-52.
[7]
Baj-Krzyworzeka M, Majka M, Pratico D, Ratajczak J, Vilaire G, Kijowski J, Reca R, Janowska-Wieczorek A, Ratajczak MZ (2002). Platelet-derived microparticles stimulate proliferation, survival, adhesion, and chemotaxis of hematopoietic cells. Exp Hematol 30(5): 450-459.
[8]
Freyssinet JM, Toti F, Hugel B, Gidon-Jeangirard C, Kunzelmann C, Martínez MC, Meyer D (1999). Apoptosis in vascular disease. Thromb Haemost 82(2): 727-735.
[9]
Tan KT, Tayebjee MH, Lynd C, Blann AD, Lip GY (2005).Platelet microparticles and soluble P selectin in peripheral artery disease: relationship to extent of disease and platelet activation markers. Ann Med 37(1): 61-66.
[10]
Shet AS, Aras O, Gupta K, Hass MJ, Rausch DJ, Saba N, Koopmeiners L, Key NS, Hebbel RP (2003). Sickle blood contains tissue factor-positive microparticles derived from endothelial cells and monocytes. Blood 102 (7): 2678-2683.
[11]
Combes V, Coltel N, Alibert M, Van Eck M, Raymond C, Juhan-Vague I, Grau GE, Chimini G (2005). ABCA1 gene deletion protects against cerebral malaria: potential pathogenic role of microparticles in neuropathology. Am J Pathol 166(1): 295-302.
[12]
Allan D, Limbrick AR, Thomas P, Westerman MP (1981). Microvesicles from sickle erythrocytes and their relation to irreversible sickling. Br J Haematol 47: 383-390
[13]
Doeuvre L, Plawinski L, Toti F, Anglés-Cano E (2009). Cell-derived microparticles: a new challenge in neuroscience. Journal of Neurochemistry 110(2): 457-468.
ADDRESS
Science Publishing Group
1 Rockefeller Plaza,
10th and 11th Floors,
New York, NY 10020
U.S.A.
Tel: (001)347-983-5186