Polymorphysm of UCP2 and H2O2 concentration to the CEC Level Variations As Predictors of Endothelial Activation In Stroke
AbstractResearch Background. Stroke as brain vascular disorder that can be ruptured vascular commonly referred to as a bleeding stroke or ischemic stroke may be due to cerebral arterial thrombosis as a final impact the progression of atherosclerosis, especially in the area of branching blood vessels. Atherogenesis related to endothelial dysfunction as a consequence shear stress exposure leads endothelial cells undergo premature senescence and activation of endothelial than occur endothelial detachment from the basement membrane as a circulating endothelial cells (CEC). Mechanism shears stress on endothelial activation can not be separated from the increased production of hydrogen peroxidase (H2O2), which will activate the PPAR-? then increase levels of free fatty acids are capable of modulating the uncoupling protein 2 (UCP 2) gene as a compensation for lowering of free fatty acids.
Reseach Methods and Results. Researchers used 40 subjects were classified into two categories on a range of healthy and sick, who then performed blood sampling edge for lipid profile analysis, CEC using flowcytometry, H2O2 measurement with ELISA techniques and DNA isolation followed by PCR procedures with the Genomic DNA that has been extracted from blood samples amplified with the 5’-GCT GCT CAC AGG TCT GCC AC-3’sebagai forward primer and 5’-AGG CGT CAG GAG ATG GAC CG-3’sebagai reverse primer (Sesti et al, 2003; Oktavianthi et al, 2012). Genotype (-866) AA is characterized by fragments of 363 bp cutting results Mlu1 sites, whereas genotypes (-866) GG marked on fragments of 295 bp and 68 bp. The equipment used was a thermal cycler (Gene Amp® PCR System 9700 [Applied Biosystems, Foster City, CA, USA]). Results showed that
Conclusion. CEC in the group sick 3 times higher than the healthy group as well as the levels of H2O2, but the two groups are not found polymorfism in both groups. Similarly, from the analysis of UCP2 gene allele frequencies between groups of stroke was not significantly different from the control group, this means yet certain UCP2 gene predispose and contribute to the pathogenesis of stroke.
2. Yu L, Haley S, Perret J, Harris M, Wilson J and Qian M. 2002. Free radical scavenging properties of wheat extracts. J Agric Food Chem.50: 1619-1624.
3. Halliwell, B., and J.M.C. Gutteridge. 1996. Free radicals in biology and medicine. Oxford University Press, Oxford.
4. Rice-Evans, C., Anthony, T.D. 1991. Techniques In Free Radical Research. Elsevier. P146-202
5. Rabelink, T. J. : Nat. Rev. Nephrol. 6, 404 – 414 (2010) Endothelial activation and circulating marker of endothelial activation in kidney disease.
6. Csiszar A, J Toth1, J Peti-Peterdi, Z Ungvari. 2007.The aging kidney: role of endothelial oxidative stress and inflammation. Acta Physiologica Hungarica. 94(1–2): 107-115
7. Van der Loo B, Labugger R, Skepper JN, Bachschmid M,
Kilo J, Powell JM, Palacios-Callender M, Erusalimsky JD, Quaschning T, Malinski T, Gygi D, Ullrich V, Luscher TF. 2000. Enhanced peroxynitrite formation is associated with vascular aging. J Exp Med.192:1731-1744
8. Griendling, K. K. and G. A. FitzGerald (2003). “Oxidative stress and cardiovascular injury: Part II: animal and human studies.” Circulation 108(17): 2034-40.
9. Brandes, Ralf P. Ingrid Fleming. Rudi Busse. 2005. Endothelial aging. Cardiovascular Research. 66: 286-294. www.elsevier.com/locate/cardiores. Downloaded on May, 28, 2013
10. Bernard I. Levy, Ernesto L. Schiffrin, Jean-Jacques Mourad, Denis Agostini, Eric Vicaut. 2008. Impaired Tissue Perfusion: A Pathology Common to Hypertension, Obesity, and Diabetes Mellitus. Circulation. 118:968-976
11. Ryu JW, Hong KH, Maeng JH, Kim JB, Ko J, Park JY, Lee KU, HongMK, Park SW, Kim YH, Han KH. 2004.Overexpression of uncoupling protein2 in THP1 monocytes inhibits beta2 integrin-mediated firm adhesion andtransendothelial migration. Arterioscler Thromb Vasc Biol. 24:864-870.
12. Piqueras L. Sanz MJ. Perretti M. Morcillo E. Norling L. Mitchell JA. Li Y. Bishop-Bailey D. 2009. Activation of PPARbeta/delta inhibits leukocyte recruitment, cell adhesion molecule expression, and chemokine release. J Leukoc Biol. 86(1):115-122
13. Chevillotte E, Giralt M, Miroux B, Ricquier D, Villarroya F. 2007.Uncouplingprotein-2 controls adiponectin gene expression in adipose tissue throughthe modulation of reactive oxygen species production. Diabetes. 56:1042-1050
14. Ouchi N, Kihara S, Arita Y, Maeda K, Kuriyama H, Okamoto Y, Hotta K, Nishida M, Takahashi M, Nakamura T, Yamashita S, Funahashi T, Matsuzawa Y. 1999. Novel modulator for endothelial adhesion molecules: adipocytederived plasma protein adiponectin. Circulation.100:2473–2476
15. Ouchi, N. Terauchi, Y. Yamauchi, T. 2000. adiponectin, an adipocytederived plasm protein, inhibits enothelial NFkB signalig through a cAMP dependent pathway. Cirulation. 102: 1296-1301
16. Kubota, N., Terauchi, Y. and Yamauchi, T. 2002. Disruption of adiponectin causes insulin resistance and neointimal formation J. Biol. Chem., 277:25863–6.
17. H. Oberkofler, B. Iglseder, K. Klein, J. Unger, M. Haltmayer, F. Krempler, B. Paulweber, W. Patsch , 2005, Associations of the UCP2 Gene Locus With Asymptomatic Carotid Atherosclerosis in Middle-Aged Women , Arterioscler Thromb Vasc Biol. 2005;25:604-610
18. Japardi, Iskandar, 2002 Japardi, 2002. Patofisiologi Stroke Infark Akibat Tromboemboli. http://library.usuac.id.
19. Lyrawati D (2009) Mitochondria powerhouse of disease: lecture for postgrad (S3) Fac. Med Brawijaya University. pdf (low res.) pdf mt-dis https://lyrawati.wordpress.com/molecular-biology/ on line
20. Michelangela Barbieri & Virginia Boccardi & Antonietta Esposito & Michela Papa & Francesco Vestini & Maria Rosaria Rizzo & Giuseppe Paolisso, 2011, A/ASP/VAL allele combination of IGF1R, IRS2, and UCP2 genes is associated with better metabolic profile, preserved energy expenditure parameters, and low mortality rate in longevity, AGE (2012) 34:235–245 DOI 10.1007/s11357-011-9210-z
21. Christoper J. Boos., 2006, Circulating endothelial cells in cardiovascular disease, Journal of American College of cardiology, Vol. 48, No.8, 2006 ISSN 0735-1097/06
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