Summary
Glycoprotein (GP) Ibα ectodomain shedding has important implications for thrombosis and hemostasis. A disintegrin and metalloproteinase 17 (ADAM17) was identified to play an essential role in agonist induced GPIbα shedding. The relationship of GPIbα shedding and ADAM17 in the acute stage of atherosclerotic ischemic stroke (AIS) patients has not been thoroughly studied. A total of 306 patients and 230 controls matched for age, sex, race, history of hypertension and diabetes mellitus were enrolled in the study. GPIbα, ADAM17, glycocalicin were detected by flow cytometry, Western blotting, and enzyme-linked immunosorbent assay (ELISA) respectively. Compared with the control group, the expression of GPIbα in patients with acute ischemic stroke was significantly lower (P=0.000, P<0.01). Plasma glycocalicin and ADAM17 in AIS group were higher than those in control group (P=0.699, P=0.000). Pearson’s analysis showed glycocalicin bore no correlation with GPIbα in AIS patients (r=0.095, P>0.05). GPIbα and National Institute of Health Stroke Scale (NIHSS) had negative correlation (r=−0.514, P<0.01). Our findings indicate that ADAM17 may be a risk factor for ischemic stroke in Chinese and the expression of GPIbα can serve as a measure for stroke severity.
Similar content being viewed by others
References
Lopez AD, Mathers CD, Ezzati M, et al. Global and regional burden of disease and risk factors, 2001: systematic analysis of population health data. Lancet, 2006, 367(9524):1747–1757
Feigin VL, Lawes CM, Bennet DA, et al. Stroke epidemiology: a review of population-based studies of incidence, prevalence, and case-fatality in the late 20th century. Lancet Neurol, 2003,2(1):43–53
Stoll G, Kleinschnitz C, Nieswandt B. The role of glycoprotein Ibalpha and von Willebrand factor interaction in stroke development. Hamostaseologie, 2010,30(3): 136–138
Bergmeier W, Piffath CL, Cheng G, et al. Tumor necrosis factor-alpha-converting enzyme (ADAM17) mediates GPIbalpha shedding from platelets in vitro and in vivo. Circ Res, 2004,95(7):677–683
White MM, Jennings LK. Platelet protocols. Research and Clinical Laboratory Procedures. San Diego: Academic Press, 1999
Zhang Y, Zhao Y, Lu S, et al. A high-throughput biotinavidin-elisa for studying expression of platelet membrane glycoproteins and its clinical application. Tohoku J Exp Med, 2010,222(1):83–88
del Zoppo GJ. The role of platelets in ischemic stroke. Neurology, 1998,51(3 Suppl 3):S9–S14
Tokuue J, Hayashi J, Hata Y, et al. Enhanced platelet aggregability under high shear stress after treadmill exercise in patients with effort angina. Thromb Haemost, 1996,75(5):833–837
Sonoda A, Murata M, Ito D, et al. Association between platelet glycoprotein Ib genotype and ischemic cerebrovascular disease. Stroke, 2000,31(2):493–497
Maguire JM, Thakkinstian A, Sturm J, et al. Polymorphisms in platelet glycoprotein 1balpha and factor VII and risk of ischemic stroke: a meta-analysis. Stroke, 2008,39(6):1710–1716
Elvers M, Stegner D, Hagedorn I, et al. Impaired αIIbβ3 integrin activation and shear-dependent thrombus formation in mice lacking phospolipase D1. Sci Signal, 2010, 3(103): ra1
Han Y, Wang Z, Zhu M, et al. Study of platelet membrane glycoproteins and its fibrinogen binding reaction in patients with cerebral infarction and diabetes mellitus. Zhonghua Xueyexue Zazhi (Chinese), 2000,21(3):129–131
Alan D. Flow cytometry: a clinical test of platelet function. J Blood, 1996, 87(12):4925–4936
Dai K, Yan R, Li S, et al. Prolonged inhibition of protein kinase A results in metalloproteinase-dependent platelet GPIba shedding. Thromb Res, 2009,124(1):101–109
Brill A, Chauhan AK, Canault M, et al. Oxidative stress activates ADAM17/TACE and induces its target receptor shedding in platelets in a p38-dependent fashion. Cardiovasc Res, 2009,84(1):137–144
Aktas B, Pozgajova M, Bergmeier W, et al. Aspirin induces platelet receptor shedding via ADAM17 (TACE). J Biol Chem, 2005,280(48):39716–39722
Stoll G, Kleinschnitz C, Nieswandt B. Combating innate inflammation: a new paradigm for acute treatment of stroke? Ann NY Acad Sci, 2010,1207:149–154
Boilard E, Nigrovic PA, Larabee K, et al. Platelets amplify inflammation in arthritis via collagen-dependent microparticle production. Science, 2010,327(5965):580–583
Beer JH, Buchi L, Steiner B. Glycocalicin: a new assay-the normal plasma levels and its potential usefulness in selected diseases. Blood, 1994,83(3):691–702
Coller BS, Kalomiris E, Steinberg M, et al. Evidence that glycocalicin circulates in normal plasma. J Clin Invest, 1984,73(3):794–799
Wang X, Feuerstein GZ, Xu L, et al. Inhibition of tumor necrosis factor-nlpha. converting enzyme by a selective antagonist protects brain from focal ischemic injury in rats. Mol Pharmacol, 2004,65(4):890–896
Hurtado O, Lizasoain I, Fernández-Tomé P, et al. TACE/ADAM17-TNFα pathway in rat cortical cultures after exposure to oxygen-glucose deprivation or glutamate. J Cereb Blood Flow Metab, 2002,22(5):576–585
Cárdenas A, Moro MA, Leza JC, et al. Up-regulation of TACE/ADAM17 after ischemic preconditioning is involved in brain tolerance. J Cere Blood Flow Metab, 2002,22(11):1297–1302
Author information
Authors and Affiliations
Corresponding author
Additional information
This project was supported by the National Natural Science Foundation of China (No. 81072945).
Rights and permissions
About this article
Cite this article
Ling, Jy., Shen, L., Liu, Q. et al. Changes in platelet GPIbα and ADAM17 during the acute stage of atherosclerotic ischemic stroke among Chinese. J. Huazhong Univ. Sci. Technol. [Med. Sci.] 33, 438–442 (2013). https://doi.org/10.1007/s11596-013-1138-3
Received:
Published:
Issue Date:
DOI: https://doi.org/10.1007/s11596-013-1138-3