Elif Erdoğan, Fatma Bahice Cinemre, Hakan Cinemre, Abdullah Tüten, Nevin Yılmaz, Barış Kaya, Birsen Aydemir

DISTRIBUTION OF SELENOPROTEIN W1 (rs3786777) GENOTYPES IN TURKISH PREECLAMPTIC WOMEN

Objective: Preeclampsia is characterized by hypertension, proteinuria and edema during pregnancy, It causes. intrauterine growth retardation, premature birth, fetal and maternal mortality. The selenium takes place in the structure of selenoproteins which are mostly showing oxidoreductase activity in human. Some studies were reported that selenoproteins W (SelW) plays an important role as an antioxidant in the developing brain and embryo. SelW expression level in the fetal muscle and heart tissue depends on fetal selenium levels. SelW function is not completely elucidated yet. The purpose of this study was to determine whether common variation in selenoprotein W1 (SEPW1) alters the risk of preeclampsia (PE). Materials and Methods: 82 pregnant women with PE and 85 healthy pregnant women from the same geographic region were included in the study. Allele-specific Polymerase Chain Reaction (ASPCR) analysis was used to identify polymorphism of the SEPW1 gene (rs3786777). Results: Serum lipids, total protein and albumin levels were measured in all cases. We found that fetal weight, total protein and albumin levels significantly decreased in preeclamptic pregnancies compared to healthy pregnant (p=0.001, for each). Systolic and diastolic blood pressure, body mass index, total cholesterol and triglyceride levels were significantly increased in preeclamptic patients when compared to healthy control group (p=0.001, p=0.001, p=0.001, p=0.05, p=0.01, respectively). The frequencies of the CC, CA and AA genotypes were found as 23 %, 67 % and 10 % in pregnant women with PE and 27 %, 57 % and 16 % in healthy pregnant women, respectively. Our results indicated that the distribution of the SEPW1 genotypes and alleles did not differ significantly among subjects with or without PE (p>0.05). Conclusions: In some study SelW is associated with fetal development, so we thought that its gene distribution may be involved in the occurrence of preeclampsia or its complication. SEPW1 polymorphism did not alter the risk of PE in our population. However, clarification by further studies in larger populations is needed. SEPW1 (rs3786777) polymorphism has no role in etiopathogenesis of preeclamptic Turkish women.

Keywords:

Preeclampsia; Selenoprotein W1 gene; Polymorphism,

PDF

___

1. Lima VJ, Andrade CR, Ruschi GE, Sass N. Serum lipid levels in pregnancies complicated by preeclampsia. Sao Paulo Med J 2011;129:73–6.
2. Benstoem C, Goetzenich A, Kraemer S et al. Selenium and Its Supplementation in Cardiovascular Disease—What do We Know? Nutrients 2015; 7:3094-118.
3. Forceville X, Mostert V, Pierantoni A et al. Selenoprotein, P. Rather than Glutathione Peroxidase, as a Potential Marker of Septic Shock and Related Syndromes. Eur. Surg. Res 2009; 43: 338–47.
4. Yang SJ, Hwang SY, Choi HY et al. Serum selenoprotein P levels in patients with type 2 diabetes and prediabetes: Implications for insulin resistance, inflammation, and atherosclerosis. J. Clin. Endocrinol. Metab 2011; 96: E1325–E1329.
5. V.N. Gladyshev, Selenoproteins and selenoproteomes, in: D.L. Hatfield, M.J. Berry, V.N. Gladyshev (Eds.), Selenium: Its Molecular Biology and Role in Human Health,2 nd ed,, Springer Science, N. Y., 2006, pp. 99–110.
6. Whanger PD. Selenoprotein expression and function-selenoprotein W. Biochim Biophys Acta 2009;1790(11): 1448-52.
7. Gu QP, Sun Y, Ream LW, Whanger PD. Selenoprotein Waccumulates primarily in primate skeletal muscle, heart, brain and tongue, Mol. Cell. Biochem 2000; 204: 49–6.
8. Butler JA, Xia Y, Zhou Y, Sun Y, Whanger PD. Selenium, cellular glutathione peroxidase and selenoprotein W in fetal tissues from deficient, adequate and excessive selenium areas of China, FASEB J 1999;13: A248.
9. Bellingham J, Gregory-Evans K, Fox MF, Gregory-Evans CY. Gene structure and tissue expression of human selenoprotein W, SEPW1, and identification of a retroprocessed pseudogene, SEPW1P, Biochim. Biophys. Acta 2003;162: 140–46.
10. Sun Y, Gu QP, Whanger PD. Selenoprotein W in overexpressed and underexpressed glial cells in culture. J Inorgan Biochem 2001;84: 151–56.
11. Loflin J, Lopez N, Whanger PD, Kioussi CJ. SelenoproteinW during development and oxidative stres. J Inorgan Biochem 2006; 100: 1679–84.
12. Kioussi CJ, Whanger PD. Selenoprotein W in development and oxidative stress, in: D.L. Hatfield, M.J. Berry, V.N. Gladyshev (Eds.), Selenium: Its Molecular Biology and Role in Human Health, 2nd ed, Springer Science, N. Y. 2006: pp. 153–181.
13. Reszka E. Selenoproteins in bladder cancer cancer. Clin Chim Acta 2012; 413(9-10): 847-54.
14. Slattery ML, Lundgreen A, Welbourn B, Corcoran C, Wolff RK. Genetic Variation in Selenoprotein Genes, Lifestyle, and Risk of Colon and Rectal Cancer. PLoS ONE 2012; 7(5): e37312.
15. Meplan C, Hesketh J. The influence of selenium and selenoprotein gene variants on colorectal cancer risk. Mutagenesis. 2012r; 27(2): 177-86.
16. ACOG practice bulletin. Diagnosis and management of preeclampsia and eclampsia. Obstet Gynecol 2002; 99:159–67.
17. Vendeland SC, Beilstein MA, Yeh JY, Ream WL, Whanger PD. Rat skeletal muscle selenoproteinW: cDNA clone and mRNA modulation by dietary selenium, Proc. Natl. Sci. USA 1995; 92: 8749–53.
18. Schubert JR, Muth OH, Oldfield JE, Remmert LF. Experimental results with selenium in white muscle disease of lambs and calves, Fed Proc 1961; 20: 689–94.
19. Gu BQ. Pathology of Keshan disease: a comprehensive review, Chin Med J 1983; 96: 251–61.
20. Shrimali RK, Irons RD, Carlson BA et al. Selenoproteins mediate T cell immunity through an antioxidant mechanism. J Biol Chem 2008; 283: 20181–185.
21. Jiang C, Hu H, Malewicz B, Wang Z, Lü J. Selenite-induced p53 Ser-15 phosphorylation and caspase-mediated apoptosis in LNCaP human prostate cancer cells. Mol Cancer Ther 2004; 3: 877–84.
22. Hawkes WC, Alkan Z. Delayed cell cycle progression from SEPW1 depletion is p53- and p21-dependent inMCF-7 breast cancer cells. Biochem Biophys Res Commun 2011; 413: 36–40.
23. Hawkes WC, Printsev I, Alkan Z. Selenoprotein W depletion induces a p53- and p21-dependent delay in cell cycle progression in RWPE-1 prostate epithelial cells. J Cell Biochem 2011; doi:10.1002/jcb.23328.
24. Jeong D, Kim TS, Chung YW, Lee BJ, Kim IY. Selenoprotein W is a glutathionedependent antioxidant in vivo. FEBS Lett 2002; 517: 225–28.
25. Pellatt AJ, Wolff RK, John EM, et al. SEPP1 Influences Breast Cancer Risk among Women with Greater Native American Ancestry: The Breast Cancer Health Disparities Study. PLoS ONE 2013; 8(11): e80554.