EFEK PAPARAN GLUKOSA KONSENTRASI TINGGI TERHADAP PENINGKATKAN AKTIVITAS ISOZIM PROTEIN KINASE C (PKC)-ALPHA PADA KULTUR SEL STROMA PROSTAT
##plugins.themes.bootstrap3.article.main##
##plugins.themes.bootstrap3.article.sidebar##
Abstract
OBJECTIVE: To prove that glucose treatment in human prostatic stromal cells (HPSC) culture would increase PKC alpha isozyme activity. MaterialS & Methods: Primary cultures of HPSC were obtained from patients with bladder outlet obstruction caused by benign prostatic enlargement. The effects of various concentrations of glucose (5, 10, 15, 20, 25, 30, 35 micro-Mol) on PKC-alpha isozyme activity were examined quantitatively by spectrophotometry methods. ResultS: Spectrophotometry analysis, which is used to assess isozyme activity quantitatively, showed that exposures to various doses of glucose resulted in increased isozyme activity. The increment of activity is linear with the increment of glucose dose. There is a strong correlation between glucose doses and PKC-alpha activity, with R2 = 0,91. Conclusion: At different concentrations glucose increases PKC-alpha isozyme activity of HPSC.
##plugins.themes.bootstrap3.article.details##
Protein kinase, human prostatic stroma cell culture, high glucose, dynamic component
Glasser DB, Carson C 3rd, Kang JH, Laumann EO. Prevalence of storage and voiding symptoms among men aged 40 years and older in a US population-based study: Results from the Male Attitudes Regarding Sexual Health study. Int J Clin Pract 2007; 61(8): 1294-300.
Roehrborn CG, McConnell JD. Etiology, pathophysiology, epidemiology, and natural history of benign prostatic hyperplasia. In: Campbell’s Urology, edisi ke 7. editor: Walsh PC, Retik AB, Vaughan ED, dan Wein AJ. Philadelphia: WB Saunders Co; 2002. p. 1297-330.
Nordling J, Artibani W, Hald T, Horn T, Keuppens F, Levin R, et al. Pathophysiology of the urinary bladder in obstruction and ageing. In: Chatelain Ch, Denis L, Foo KT, Khoury S, Mc Connell J (editors). Benign prostatic hyperplasia. 5th International consultation on BPH. London: Health Publication Ltd; 2001. p. 519-35.
Michel MC, Mehlburger L, Schumacher H, Bressel H, Goepel M. Effect of diabetes on lower urinary tract symptoms in patients with benign prostatic hyperplasia. J. Urol 2000; 163: 1725–9.
Öztürk Y, Altan VM, Yildizoglu-Ari N. Effects of experimental diabetes and insulin on smooth muscle functions. Pharmacol Rev. 1996; 48: 69.
Boon TA, Van Venrooij GE, Eckhardt MD. Effect of diabetes mellitus on lower urinary tract symptoms and dysfunction in patients with benign prostatic hyperplasia. Curr Urol Rep 2001; 2(4): 297-301.
Ramasamy S, Hodgson WC, Ventura S. Protein kinase C and the sub-sensitivity and sub-reactivity of the diabetic rat prostate gland to noradrenaline. European Journal of Pharmacology 2002; 434: 151– 61.
Wang ZJ, Ikeda K, Wada Y, Foster Jr HE, Weiss RM, Latifpour J. Expression and location of basic fibroblast growth factor in diabetic rat prostate. BJU International 2000; 85: 945-52.
Ikeda K, Wada Y, Foster Jr HE, Wang JY, Weiss RM, Latifpur J. Experimental diabetes-induced regression of the rat prostate is associated with an increased expression of transforming growth factor-betha. J Urol 2000; 164: 180-5.
Itoh H, Yamamura S, Ware JA, Zhuang S, Mii S, Liu B, et al. Differential effect of protein kinase C on human vascular smooth muscle cell proliferation and migration. Am J Physiol Heart Circ Physiol 2001; 281: H359-H370.
Guh JH, Hwang TL, Ko FN, Chueh SC, Lai MK, Teng CM. Antiproliferative effect in human prostatic smooth muscle cells by nitric oxide donor. Mol Pharm 1998; 53: 467-74.
Kamp TJ, Hell JW. Regulation of cardiac L-Type calcium channels by protein kinase A and protein kinase C. Circ Res 2000; 87: 1095-102.
Preston A, Haynes JM. Alpha1-Adrenoceptor efects mediated by protein kinase C a in human cultured prostatic stromal cells. Brit Jour of Pharmacology 2003; 138: 218–24.
Hiramatsu Y, Sekiguchi N, Hayashi M, Isshiki K. Diacylglycerol and protein kinase C activity are increased in mouse model of diabetic embryopathy. Diabetes 2002; 41: 2804-10.
Koya D, King GL. Protein kinase C kinase activation and development of diabetic complication. Diabetes 1998; 47 (6): 859-66.
William B, Schreier RW. Characterization of glucose-induced in situ protein kinase C activity in cultured vascular smooth muscle cells. Diabetes 1992; 41 (11): 1464-72.
Dewi N. Karakterisasi ekstrak kasar enzim protein kinase C-α hasil isolasi dari serum darah penderita pre-ekalmsia. Skripsi. Unibraw; 2000.
Waring JV, Wendt IR. Effects of streptozotocin- induced diabetes mellitus on intracellular calcium and contraction of longitudinal smooth muscle from rat urinary blafdder. J Urol 2000; 163: 323-30.
Bezuijen MWF, Levendusky MC, Longhurst PA. Functional response of bladder strips from streptozotocin diabetic rats on bladder mass. J Urol 2003; 169: 2397-401.
Liu X, Wang J, Takeda N, Binaglia L, Panagia V, Dhalla NS. Changes in cardiac protein kinase C activties and isozymes in streptozocin-induced diabetes. Am J Physiol (Endocrinol Metab. 40) 1999; 277: E798-E804.
Inoguchi T, Li P, Umeda F. High glucose level and free fatty acid stimulate reactive oxygen species production through protein kinase C-dependent activation of NAD(P)H oxidase in culture vascular cells. Diabetes 2000; 49: 1939-45.
Muniyappa R, Srinivas PR, Ram JL, Walsh MF, Sowers JR. Calcium and protein kinase C mediate high glucose-induced inhibition of inducible nitric oxide synthase in vascular smooth muscle cells. Hypertension 1998, 31 (part2): 289-95.
Cartledge JJ, Eardley I, Morrison JFB. Advanced glycation end products are responsible for the impairement of corpus cavernosal smooth muscle relaxation in diabetes. BJU International 2001; 87: 401-7.