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TGF-β1 869T/C Polymorphism and Ischemic Stroke: Sex Difference in Chinese

Published online by Cambridge University Press:  23 September 2016

Hong-miao Tao*
Affiliation:
School of Medicine, Jinhua College of Profession & Technology
Guo-zhong Chen
Affiliation:
School of Medicine, Jinhua College of Profession & Technology
Xiao-dong Lu
Affiliation:
Department of Clinical Laboratory, Jinhua Central Hospital
Gan-ping Chen
Affiliation:
Department of Neurology, Jinhua Peoples Hospital, Jinhua
Bei Shao
Affiliation:
Cerebrovascular Unit, Department of Neurology, the First Affiliated Hospital, Wenzhou Medical College, Wenzhou, Zhejiang Province, the People's Republic of China
*
School of Medicine, Jinhua College of Profession & Technology, Jinhua, 321007, Zhejiang Province, the People's Republic of China
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Abstract

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Background:

Inflammation plays a pivotal role in the pathogenesis of atherosclerosis and of cerebrovascular complications. Transforming growth factor-β (TGF-β) is a pleiotropic cytokine with a central role in inflammation. To investigate whether polymorphisms of the TGF-β1 gene can modify the risk of ischemic stroke (IS) in Chinese population, we conduct this hospital-based, case-control study.

Methods:

Transforming growth factor-β1 genotype was determined in 450 Chinese patients (306 male and 144 female) with IS and 450 control subjects (326 male and 124 female).

Results:

Subjects carrying 869TT were susceptible to IS (odds ratio [OR] =1.58; P=0.003). Further analysis of IS data partitioned by gender revealed the female-specific association with 869T/C (OR=2.64; P=0.001).

Conclusions:

Findings suggest that the TT genotype of 869T/C might be a risk factor of IS in Chinese, especially in females.

Résumé

RésuméContexte:

L'inflammation joue un rôle clé dans la pathogenèse de l'athérosclérose et des complications cérébrovasculaires. Le facteur de croissance transformant β (TGF-β) est une cytokine pléiotrope qui joue un rôle central dans l'inflammation. Nous avons effectué cette étude cas témoins en milieu hospitalier afin de déterminer si les polymorphismes du gène TGF-β1 pouvaient influencer le risque d'accident vasculaire cérébral ischémique (AVCI) dans la population chinoise.

Méthodologie:

Le génotype TGF-β1 a été déterminé chez 450 patients Chinois (306 hommes et 144 femmes) atteints d'AVCI et chez 450 témoins (326 hommes et 124 femmes).

Résultats:

Les sujets porteurs de 869TT étaient plus à risque d'AVCI (RC 1,58 ; p = 0,003). L'analyse des données selon le sexe a montré une association avec 869T/C chez les femmes (RC 2,64 ; p = 0,001).

Conclusions:

Selon ces résultats, le génotype TT de 869T/C pourrait être un facteur de risque de l'AVCI chez les Chinois, surtout chez les femmes.

Type
Original Articles
Copyright
Copyright © The Canadian Journal of Neurological 2010

References

1. World Health Organization. The World Health Report: shaping the future. Geneva, Switzerland: WHO; 2003.Google Scholar
2. Hassan, A, Markus, HS. Genetics and ischaemic stroke. Brain. 2000; 123(Pt 9):1784–812.10.1093/brain/123.9.178410960044Google Scholar
3. Libby, P. Inflammation in atherosclerosis. Nature. 2002; 420(6917):868–74.10.1038/nature0132312490960Google Scholar
4. Kim, JS, Yoon, SS, Kim, YH, Ryu, JS. Serial measurement of interleukin-6, transforming growth factor-beta, and S-100 protein in patients with acute stroke. Stroke. 1996; 27(9):1553–7.10.1161/01.STR.27.9.15538784129Google Scholar
5. Li, D, Liu, Y, Chen, J, et al. Suppression of atherogenesis by delivery of TGFbeta1ACT using adeno-associated virus type 2 in LDLR knockout mice. Biochem Biophys Res Commun. 2006;344(3):701–7.10.1016/j.bbrc.2006.04.01016631603Google Scholar
6. Grainger, DJ. Transforming growth factor beta and atherosclerosis: so far, so good for the protective cytokine hypothesis. Arterioscler Thromb Vasc Biol. 2004; 24(3):399404.10.1161/01.ATV.0000114567.76772.3314699019Google Scholar
7. Robertson, AK, Rudling, M, Zhou, X, Gorelik, L, Flavell, RA, Hansson, GK. Disruption of TGF-βsignaling in T cells accelerates atherosclerosis. J Clin Invest. 2003; 112(9):1342–50.10.1172/JCI1860714568988Google Scholar
8. Tashiro, H, Shimokawa, H, Sadamatu, K, Yamamoto, K. Prognostic significance of plasma concentrations of transforming growth factor-βin patients with coronary artery disease. Coron Artery Dis. 2002;13(3):139–43.10.1097/00019501-200205000-0000112131016Google Scholar
9. Bobik, A. Transforming growth factor-betas and vascular disorders. Arterioscler Thromb Vasc Biol. 2006; 26(8):1712–20.10.1161/01.ATV.0000225287.20034.2c16675726Google Scholar
10. Singh, NN, Ramji, DP. The role of transforming growth factor-beta in atherosclerosis. Cytokine Growth Factor Rev. 2006; 17(6):487–99.10.1016/j.cytogfr.2006.09.00217056295Google Scholar
11. Fujii, D, Brissenden, JE, Derynck, R, Francke, U. Transforming growth factor beta gene maps to human chromosome 19 long arm and to mouse chromosome 7. Somat Cell Mol Genet. 1986; 12(3):281–8.10.1007/BF015707873459257Google Scholar
12. Awad, MR, El-Gamel, A, Hasleton, P, Turner, DM, Sinnott, PJ, Hutchinson, IV. Genotypic variation in the transforming growth factor-beta1 gene: association with transforming growth factor-beta1 production, fibrotic lung disease, and graft fibrosis after lung transplantation. Transplantation. 1998; 66(8):1014–20.10.1097/00007890-199810270-000099808485Google Scholar
13. Shah, R, Rahaman, B, Hurley, CK, Posch, PE. Allelic diversity in the TGFB1 regulatory region: characterization of novel functional single nucleotide polymorphisms. Hum Genet. 2006; 119(1–2):6174.10.1007/s00439-005-0112-y16369764Google Scholar
14. Lu, LY, Cheng, HH, Sung, PK, Yeh, JJ, Shiue, YL, Chen, A. Singlenucleotide polymorphisms of transforming growth factor-beta1 gene in Taiwanese patients with systemic lupus erythematosus. J Microbiol Immunol Infect. 2004; 37(3):145–52.15221033Google Scholar
15. Yang, ZX, Wang, H, Gao, CF, Xu, LL, Zhao, WJ. Effect of polymorphisms of transforming growth factor B1 gene on HBV-induced liver cirrhosis. Natl Med J China. 2005; 85(15):1021–6.Google Scholar
16. Grainger, DJ, Heathcote, K, Chiano, M, et al. Genetic control of the circulating concentration of transforming growth factor type beta1. Hum Mol Genet. 1999; 8(1):93–7.10.1093/hmg/8.1.939887336Google Scholar
17. Dunning, AM, Ellis, PD, McBride, S, et al. A transforming growth factorbeta1 signal peptide variant increases secretion in vitro and is associated with increased incidence of invasive breast cancer. Cancer Res. 2003; 63(10):2610–5.12750287Google Scholar
18. Yokota, M, Ichihara, S, Lin, TL, Nakashima, N, Yamada, Y. Association of a T29––>C polymorphism of the transforming growth factor-beta1 gene with genetic susceptibility to myocardial infarction in Japanese. Circulation. 2000; 101(24):2783–7.10.1161/01.CIR.101.24.278310859282C+polymorphism+of+the+transforming+growth+factor-beta1+gene+with+genetic+susceptibility+to+myocardial+infarction+in+Japanese.+Circulation.+2000;+101(24):2783–7.10.1161/01.CIR.101.24.278310859282>Google Scholar
19. The International HapMap Consortium. The International HapMap Project. Nature. 2003; 426:789–96.10.1038/nature0216814685227Google Scholar
20. Kim, Y, Lee, C. The gene encoding transforming growth factor beta 1 confers risk of ischemic stroke and vascular dementia. Stroke. 2006;37(11):2843–5.10.1161/01.STR.0000244782.76917.8716990569Google Scholar
21. Sie, MP, Uitterlinden, AG, Bos, MJ, et al. TGF-beta 1 polymorphisms and risk of myocardial infarction and stroke: the Rotterdam Study. Stroke. 2006; 37(11):2667–71.10.1161/01.STR.0000244779.30070.1a17023672Google Scholar
22. Carter, AM, Catto, AJ, Bamford, JM, Grant, PJ. Gender-specific associations of the fibrinogen B beta 448 polymorphism, fibrinogen levels, and acute cerebrovascular disease. Arterioscler Thromb Vasc Biol. 1997; 17(3):589–94.10.1161/01.ATV.17.3.5899102181Google Scholar
23. Schurks, M, Zee, RY, Buring, JE, Kurth, T. Interrelationships among the MTHFR 677C>T polymorphism, migraine, and cardiovascular disease. Neurology. 2008; 71(7):505–13.10.1212/01.wnl.0000316198.34558.e518672474T+polymorphism,+migraine,+and+cardiovascular+disease.+Neurology.+2008;+71(7):505–13.10.1212/01.wnl.0000316198.34558.e518672474>Google Scholar
24. Morrison, AC, Ballantyne, CM, Bray, M, Chambless, LE, Sharrett, AR, Boerwinkle, E. LPL polymorphism predicts stroke risk in men. Genet Epidemiol. 2002; 22(3):233–42.10.1002/gepi.019111921083Google Scholar
25. Investigation committee of guideline for diagnosis and treatment of hyperlipemias, Japan Atherosclerosis Society. Guideline for diagnosis and treatment of hyperlipemias in adults. J Jpn Atheroscler Soc. 1997; 25:134.Google Scholar
26. World Health Organization Study Group Diabetes mellitus. WHO Tech Rep Ser. 1985; 727:1104.Google Scholar
27. Newton, CR, Graham, A, Heptinstall, LE, et al. Analysis of any point mutation in DNA. The amplification refractory mutation system (ARMS). Nucleic Acid Res. 1989, 17:2503–16.10.1093/nar/17.7.25032785681Google Scholar
28. Fukuda, K, Yao, H, Ibayashi, S, et al. Ovariectomy exacerbates and estrogen replacement attenuates photothrombotic focal ischemic brain injury in rats. Stroke. 2000; 31(1):155–60.10.1161/01.STR.31.1.15510625732Google Scholar
29. Santizo, RA, Xu, HL, Ye, S, Baughman, VL, Pelligrino, DA. Loss of benefit from estrogen replacement therapy in diabetic ovariectomized female rats subjected to transient forebrain ischemia. Brain Res. 2002; 956(1):8695.10.1016/S0006-8993(02)03484-412426050Google Scholar
30. Falkeborn, M, Persson, I, Terent, A, Adami, HO, Lithell, H, Bergstrom, R. Hormone replacement therapy and the risk of stroke. Follow-up of a population-based cohort in Sweden. Arch Intern Med. 1993; 153(10):1201–9.10.1001/archinte.1993.004101000350058388207Google Scholar
31. Finucane, FF, Madans, JH, Bush, TL, Wolf, PH, Kleinman, JC. Decreased risk of stroke among postmenopausal hormone users. Results from a national cohort. Arch Intern Med. 1993; 153(1):73–9.10.1001/archinte.1993.004100100970088422201Google Scholar
32. Matsuda, t, Yamamoto, T, Muraguchi, A, Saatcioglu, F. Cross-talk between transforming growth factor-B and estrogen receptor signaling through Smad3. J Biol Chem. 2001; 276:42908–14.10.1074/jbc.M10531620011555647Google Scholar