Abstract
Objective
To study the distribution of gelsolin in human platelet and plasma, and the association with blood-stasis syndrome (BSS) of coronary heart disease (CHD).
Methods
Sixty patients with CHD (30 in BSS group and 30 in non-BSS group) and 30 healthy subjects (control group) were included in this study. The classification of the syndrome was based on clinical symptoms and signs. Gelsolin concentration in platelet rich plasma (PRP), platelet poor plasma (PPP), filamentous actin (F-actin) and group-specific component globulin (Gc-globulin) of PPP were determined by enzyme-linked immunosorbent assay (ELISA). The fluorescence intensity of CD62p and cytoplasmic calcium ([Ca2+]i) in human platelets of patients and healthy persons was measured with flow cytometry.
Results
Compared with the control group, gelsolin in PRP of the BSS group increased significantly (P<0.01), while that in PPP of the BSS and non-BSS groups decreased markedly (P<0.05), the CD62p, [Ca2+]i of platelet, F-actin, and Gc-globulin of the BSS and non-BSS groups increased significantly (P<0.01). Compared with the non-BSS group, the gelsolin concentration in PRP of BSS group increased significantly (P<0.01), the [Ca2+]i of platelet of the BSS group increased markedly (P<0.01), while the F-actin and Gc-globulin of the BSS group had no statistical defference (P>0.05).
Conclusions
Gelsolin concentration in PRP was increased and accompanied by the elevated [Ca2+]i of platelet in CHD with BSS, while gelsolin in PPP were lowered markedly. We speculate that plasma gelsolin may clear F-actin from circulation, thus resulting in depletion of plasma gelsolin significantly. This, in addition to the increased calcium influx of platelets, may lead to the gelsolin abnormal expression on platelets during the process of BSS in CHD. Therefore, platelet gelsolin may serve as a new potential biomarker and a therapeutic target of BSS in CHD.
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References
Davi G, Patrono C. Platelet activation and atherothrombosis. N Engl J Med 2007;357:2482–2494.
Moliterno DJ. Advances in antiplatelet therapy for ACS and PCI. J Interv Cardiol 2008;21(S11):S18–S24.
García A. Clinical proteomics in platelet research: challenges ahead. J Thromb Haemost 2010;8:1784–1785.
Thiele T, Steil L, Gebhard S, Scharf C, Hammer E, Brigulla M, et al. Profiling of alterations in platelet proteins during storage of platelet concentrates. Transfusion 2007;47:1221–1233.
Banfi C, Brioschi M, Marenzi G, De Metrio M, Camera M, Mussoni L, et al. Proteome of platelets in patients with coronary artery disease. Exp Hematol 2010;38:341–350.
Senzel L, Gnatenko DV, Bahou WF. The platelet proteome. Curr Opin Hematol 2009;16:329–333.
Chen KJ, Xue M, Yin HJ. The relationship between platelet activation and coronary heart disease and blood-stasis syndrome. J Capital Med Univ (Chin) 2008;29:266–269.
Xue M, Chen KJ, Yin HJ. Relationship between platelet activation related factors and polymorphism of related genes in patients with coronary heart disease of bloodstasis syndrome. Chin J Integr Med 2008;14:267–273.
Li XF, Jiang YR, Wu CF, Chen KJ, Yin HJ. Study on the correlation between platelet function proteins and symptom complex in coronary heart disease. Mol Cardiol China (Chin) 2009;9:326–331.
Chen HZ, ed. Practical internal medicine. 12th ed. Beijing: People’s Medical Publishing House; 2005:1472–1473.
Society of Cardiology, Chinese Association of the Integrative Medicine. The diagnostic criteria of Chinese medicine in coronary heart disease. Chin J Integr Tradit West Med (Chin) 1991;11:257.
Zhuang MM, Wen YX, Liu SL, Hong XP. Determination of the level of cytopplasmic free calcium in human platelets with flow cytometry. J Xi’an Jiaotong Univ (Med Sci, Chin) 2005;26:508–510.
Grynkiewicz G, Poenie M, Tsien RY. A new generation of Ca2+ indicators with greatly improved fluorescence properties. J Biol Chem 1985;260:3440–3450.
Brydon L, Magid K, Steptoe A. Platelets, coronary heart disease, and stress. Brain Behav Immun 2006;20:113–119.
Antoniades C, Bakogiannis C, Tousoulis D, Demosthenous M, Marinou K, Stefanadis C. Platelet activation in atherogenesis associated with low-grade inflammation. Inflamm Allergy Drug Targets 2010;9:334–345.
Yin HL, Stossel TP. Control of cytop lasmic actin gelsol transformation by gelsolin, a calcium dependent regulatory protein. Nature 1979;281:583–586.
Spinardi L, Witke W. Gelsolin and diseases. Subcell Biochem 2007;45:55–69.
Vasconcellos CA, Lind SE. Coordinated inhibition of actin-induced platelet aggregation by plasma gelsolin and vitamin D-binding protein. Blood 1997;82:3648–3657.
Lee WM, Galbraith RM. The extracellular actin scavenger systern and actin toxicity. N Engl J Med 1992;326:1335–1341.
Suhler E, Lin W, Yin HL. Decreased plasma gelsolin concentrations in acute liver failure, myocardial infarction, septic shock and myonecrosis. Crit Care Med 1997;25:594–598.
Kato M, Kambe M, Kajiyama G. Increased cytosolic free Mg2+ and Ca2+ in platelets of patients with vasospastic. Am J Physiol 1998;274:548–554.
Fujinishi A, Takahara K, Ohba C, Nakashima Y, Kuroiwa A. Effects of nisoldipine on cytosolic calcium, platelet aggregation, and coagulation/fibrinolysis in patients with coronary artery disease. Angiology 1997;48:515–521.
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Supported by the National Natural Science Foundation of China (No. 81073086)
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Liu, Y., Yin, Hj. & Chen, Kj. Research on the correlation between platelet gelsolin and blood-stasis syndrome of coronary heart disease. Chin. J. Integr. Med. 17, 587–592 (2011). https://doi.org/10.1007/s11655-011-0814-z
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DOI: https://doi.org/10.1007/s11655-011-0814-z