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The Comparison of Maximal Platelet Aggregation in the Presence of Disperse Primary and Monolayer Secondary HUVEC Exposed to Testosterone in High Glucose Medium


Affiliations
1 Department of Physiology, Universitas Muhammadiyah Yogyakarta, Indonesia
2 Department of Anatomy and Embryology, Universitas Gadjah Mada, Yogyakarta, Indonesia
3 Department of Clinical Pathology, Universitas Gadjah Mada, Yogyakarta, Indonesia
4 Department of Physiology, Universitas Gadjah Mada, Yogyakarta, Indonesia
 

To explore in vitro models in examining the influence of testosterone (T) to platelet activation through endothelial cells in hyperglycemia condition. Disperse primary and monolayer secondary human umbilical vein endothelial cells (HUVEC) in high glucose (HG) medium were exposed to T. Maximal platelet aggregation in the presence of HUVEC was measured using turbidimetric method. Maximal platelet aggregation in the presence of disperse primary HUVEC exposed to 0, 1, 10, and 100 nM of T were 69.4%, 65.4%, 67.6%, and 62.05%, whereas of monolayer secondary HUVEC were 46.5%, 43.9%, 48.1%, and 37.45%, respectively. Maximal platelet aggregation was significantly lower (p = 0.0001) in disperse primary HUVEC than in monolayer secondary HUVEC. The two methods were moderately correlated (r = 0.06; p = 0.079) in terms of endothelial activation.Maximal platelet agregation in the presence of disperse primary HUVEC is higher than, but correlated to, of monolayer secondary HUVEC, which is exposed to T in HG medium.

Keywords

Platelet Aggregation, Endothelial Cells, Testosterone, High Glucose, In Vitro.
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  • Liu P, Death AK and Handelsman DJ. (2003) Androgens and Cardiovascular Disease. Endocr Rev. 24(3), 313-340.
  • Wu FCW and von Eckardstein A. (2003) Androgens and coronary artery disease. Endocr Rev. 24, 183-217.
  • Cines DB, Pollak ES, Buck CA, Loscalzo J, Zimmerman GA, McEver RP et al. (1998) Endothelial Cells in Physiology and in the Pathophysiology of Vascular Disorders. Blood. 91, 3527-3561.
  • Nachman RL and Jaffe EA. (2004) Endothelial cell culture: beginnings of modern vascular biology. J. Clin. Invest. 114, 1037–1040.
  • Galley HF and Webster NR. (2004) Physiology of the endothelium. Br J of Anaesthesia. 93 (1), 105-113.
  • Lagarde M, Felisi O, Boukhchache, D, Sicard, B and Dechavanne M. (1984) Relationship between cyclic AMP and thromboxane formation in platelet-endothelial cell interactions. Thromb Res. 25, 141-147.
  • Nordoy A, Svensson B and Hoa JC. (1978) The inhibitory effect of human endothelial cell monolayers on platelet reactions and its inhibition by aspirin. Thromb Res. 12, 597-608.
  • Altorjay I, Kirchmaier CM and Breddin HK. (1999) Changes of spontaneous and induced platelet aggregation in the presence of a human endothelial cell monolayer. Thromb Res. 55, 69-77.
  • Popov D. (2010) Endothelial cell dysfunction in hyperglycemia: Phenotypic change, intracellular signaling modification, ultrastructural alteration, and potential clinical outcomes. Int J Diabetes Mellitus. 2, 189–195.
  • Mijares AH, Malpartida KH, Izquierdo ES, Banuls C, Rocha M, Martinez MJG. et al. (2010) Testosterone levels in males with type 2 diabetes and their relationship with cardiovascular risk factors and cardiovascular disease. J Sex Med 7, 1954–1964.
  • Tanaka A. (1994) Primary Culture of HUVEC. Department of Obstetric and Gynecology, Kobe University School of Medicine.
  • Hatakeyama H, Nishizawa M, Nakagawa A, Nakano S, Kigoshi T and Uchida K. (2002) Testosterone inhibits tumor necrosis factor-α-induced vascular cell adhesion molecule-1 expression in human aortic endothelial cells. FEBS Lett. 530, 129-132.
  • Ling S, Dai A, Williams MRI, Myles K, Dilley RJ, Komesaroff PA et al. (2002) Testosterone (T) enhances apoptosis-related damage in human vascular endothelial cells. Endocrinology. 143(3), 1119-1125.
  • Mukherjee TK, Dinh H, Chauduri G and Nathan L. (2002) Testosterone attenuates expression of vascular cell adhesion molecule-1 by conversion to estradiol by aromatase in endothelial cells: Implications in atherosclerosis. Proc Natl Acad Sci USA, 99(6), 4055-4060.
  • Zhang X, Wang LY, Jiang TY, Zhang HP, Dou Y, Zhao JH. et al. (2002) Effects of testosterone and 17-υ-estradiol on TNF-α-induced E-selectin and VCAM-1 expression in endothelial cells: analysis of the underlying receptor pathways. Life Sciences. 17, 15-29.
  • Jin H, Lin J, Mei YF, Peng G, Tan X, Wang DM. et al. (2007) Physiological testosterone stimulates tissue plasminogen and activator and tissue factor pathway inhibitor and inhibits plasminogen activator inhibitor type 1 release in endothelial cells. Biochem Cell Biol. 85, 246-251.
  • Goglia L, Tosi V, Sanchez AM, Flamini MI, Fu XD, Zullino S. et al. (2010) Endothelial regulation of eNOS, PAI-I, and t-PA by testosterone and dihydrotestosterone in vitro and in vivo. Mol Hum Reprod. 16(10), 761-769.
  • Campelo AE, Cutini PH and Massheimer VL. (2012) Testosterone modulates platelet aggregation and endothelial cell growth through nitric oxide pathway. J Endocrinol. 213, 77-87.
  • Giorgi EP and Stein WD. (1981) The transport of steroids into animal cells in culture. Endocrinology. 108(2), 688-697.

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  • The Comparison of Maximal Platelet Aggregation in the Presence of Disperse Primary and Monolayer Secondary HUVEC Exposed to Testosterone in High Glucose Medium

Abstract Views: 511  |  PDF Views: 161

Authors

Ikhlas Muhammad Jenie
Department of Physiology, Universitas Muhammadiyah Yogyakarta, Indonesia
Soedjono Aswin
Department of Anatomy and Embryology, Universitas Gadjah Mada, Yogyakarta, Indonesia
Budi Mulyono
Department of Clinical Pathology, Universitas Gadjah Mada, Yogyakarta, Indonesia
Kadarsih Soejono
Department of Physiology, Universitas Gadjah Mada, Yogyakarta, Indonesia

Abstract


To explore in vitro models in examining the influence of testosterone (T) to platelet activation through endothelial cells in hyperglycemia condition. Disperse primary and monolayer secondary human umbilical vein endothelial cells (HUVEC) in high glucose (HG) medium were exposed to T. Maximal platelet aggregation in the presence of HUVEC was measured using turbidimetric method. Maximal platelet aggregation in the presence of disperse primary HUVEC exposed to 0, 1, 10, and 100 nM of T were 69.4%, 65.4%, 67.6%, and 62.05%, whereas of monolayer secondary HUVEC were 46.5%, 43.9%, 48.1%, and 37.45%, respectively. Maximal platelet aggregation was significantly lower (p = 0.0001) in disperse primary HUVEC than in monolayer secondary HUVEC. The two methods were moderately correlated (r = 0.06; p = 0.079) in terms of endothelial activation.Maximal platelet agregation in the presence of disperse primary HUVEC is higher than, but correlated to, of monolayer secondary HUVEC, which is exposed to T in HG medium.

Keywords


Platelet Aggregation, Endothelial Cells, Testosterone, High Glucose, In Vitro.

References