Acta Scientific Gastrointestinal Disorders (ASGIS)(ISSN: 2582-1091)

Research Article Volume 5 Issue 2

Investigation of the Frequency of STOX1 Y153H Polymophism in Patients with Preeclampsia

Evrim Suna Arikan Söylemez1*, Dağıstan Tolga Arıöz2, Müjgan Özdemir Erdoğan3, Fatih Çelik2 and Mariam Chkhikvadze2

1Department of Medical Biology, Faculty of Medicine, Afyonkarahisar Health Sciences University, Afyonkarahisar, Turkey

2Department of Obstetrics and Gynecology, Faculty of Medicine, Afyonkarahisar Health Sciences University, Turkey

3Department of Medical Genetic, Faculty of Medicine, Afyonkarahisar Health Sciences University, Turkey

*Corresponding Author: Evrim Suna Arikan Söylemez, Department of Medical Biology, Faculty of Medicine, Afyonkarahisar Health Sciences University, Afyonkarahisar, Turkey.

Received: January 17, 2022; Published: January 24, 2022

Abstract

Preeclampsia (PE), one of the most serious complications of pregnancy, is characterized by endothelial dysfunction and hypertension. Gastrointestinal complications of preeclampsia can occur and have the risk of being life-threatening for the mother and fetus. Genetic predisposition is a risk factor for PE. In this context, the genotype rates and allele frequencies of the STOX1 gene rs1341667 (Y153H) polymorphism in peripheral blood and placental tissues (decidua, umblical cord) of 25 PE patients and 25 healthy controls were examined by Light Cycler® Nano Real Time PCR Instrument (Roche Applied Systems). The STOX1 gene rs1341667 polymorphism exists in three different genotypes in humans: TT (wild type), TC (heterozygous) and CC (mutant). When the genotype frequencies of peripheral blood and placenta samples were compared between patients and controls, there was no difference (P > 0.05). The genotype results of the decidua and umblical cord samples, analyzed from the same placenta in all cases, were the same. There was no difference between allele frequencies of the patients and controls (P > 0.05). In our study, rs1341667 polymorphism was detected in peripheral blood and placental tissues of preeclamptic mothers. However, this polymorphism was also detected in healthy pregnant women peripheral bloods and their placental tissues. There was no difference between the frequencies of the C allele, which is the risk allele, in both blood and placental tissues of controls and PE patients. In this regard, we cannot support the view that the relevant polymorphism predisposes to preeclampsia. However, our study has small number of patients. This polymorphism needs to be analyzed in large populations.

Keywords: Preeclampsia; STOX1; Y153H; rs1341667; Polymorphism

References

  1. Akiri G., et al. “Regulation of vascular endothelial growth factor (VEGF) expression is mediated by internal initiation of translation and alternative initiation of transcription”. Oncogene2 (1998): 227-236.
  2. Redman CW., et al. “Latest advances in understanding preeclampsia”. Science5728 (2005): 1592-1594.
  3. Sibai BM. “Thrombophilia and severe preeclampsia: time to screen and treat in future pregnancies?” Hypertension6 (2005): 1252-1253.
  4. Sibai BM. “Hypertension in pregnancy”. The New England Journal of Medicine 10 (1992): 733-734.
  5. ACOG practice bulletin. “Diagnosis and management of preeclampsi and eclampsia”. Number 33, January 2002. American College of Obsteticians and Gynecologists. International Journal of Gynecology and Obstetrics 1 (2002): 67-75.
  6. Baijnath S., et al. “The optimization of a chronic nitric oxide synthase (NOS) inhibition model of pre-eclampsia by evaluating physiological changes”. European Journal of Obstetrics and Gynecology and Reproductive Biology 71 (2014): 5.
  7. Powe CE., et al. “Preeclampsia, a disease of the maternal endothelium: the role of anti-angiogenic factors and implications for later cardiovascular disease”. Circulation24 (2011): 1-27.
  8. Tomimatsu T., et al. “Preeclampsia: maternal systemic vascular disorder caused by generalized endothelial dysfunction due to placental antiangiogenic factors”. International Journal of Molecular Sciences 4246 (2019).
  9. Dekker G., et al. “Etiology of preeclampsia: an update”. Journal of the Medical Association of Thailand 3 (2004): 96-103.
  10. Burton GJ., et al. “Pre-eclampsia: pathophysiology and clinical implications”. BMJl2381 (2019).
  11. English FA., et al. “Risk factors and effective management of preeclampsia”. Integrated Blood Pressure Control7 (2015).
  12. Romero R., et al. “Preeclampsia: a link between trophoblast dysregulation and an antiangiogenic state”. Journal of Clinical Investigation 123 (2013): 2775-2777.
  13. Youssef GS. “Hypertension in pregnancy”. European Society of Cardiology 17 (2019): 1-8.
  14. Ersch J., et al. “Feeding problems in preterm infants of preeclamptic mothers”. Journal of Paediatrics and Child Health 11 (2008): 651-655.
  15. Vikse BE., et al. “Preeclampsia and the risk of end-stage renal disease”. The New England Journal of Medicine 359.8 (2008): 800-809.
  16. Barton JR., et al. “Gastrointestinal complications of pre-eclampsia”. Seminars in Perinatology 3 (2009): 179-188.
  17. https://www.genecards.org/cgi-bin/carddisp.pl?gene=STOX1
  18. Oudejans CBM., et al., “The parent-of-origin effect of 10q22 in pre-eclamptic females coincides with two regions clustered for genes with downregulated expression in androgenetic placentas”. Molecular Human Reproduction8 (2004): 589-598.
  19. van Dijk M., et al. “Maternal segregation of the Dutch preeclampsia locus at 10q22 with a new member of the winged helix gene family”. Nature Genetics 37 (2005): 514-519.
  20. van Dijk M., et al. “Differential methylation of STOX1 in human placenta”. Epigenetics8 (2010): 736-742.
  21. Lachmeijer, A.M., et al. “Searching for preeclampsia genes: the current position”. European Journal of Obstetrics and Gynecology and Reproductive Biology 105 (2002): 94-113.
  22. Iglesias-Platas I., et al., “STOX1 is not imprinted and is not likely to be involved in preeclampsia”. Nature Genetics 39 (2007): 279-280.
  23. Zhao YM., et al. “Correlation between the expression of STOX1 in placenta of patients with early onset preeclampsia”. Zhonghua yi xue za zhi21 (2019): 1664-1668.
  24. Pinarbasi E., et al. “STOX1 gene Y153H polymorphism is associated with early-onset preeclampsia in Turkish population”. Gene 754 (2020): 144894.
  25. Berends AL., et al. “STOX1 gene in preeclampsia and intrauterine growth restriction”. BJOG9 (2007): 1163-1167.
  26. Kivinen K., et al. “Evaluation of STOX1 as a preeclampsia candidate gene in a population-wide sample”. European Journal of Human Genetics 15 (2007): 494-497.

Citation

Citation: Evrim Suna Arikan Söylemez., et al. “Investigation of the Frequency of STOX1 Y153H Polymophism in Patients with Preeclampsia". Acta Scientific Gastrointestinal Disorders 5.2 (2022): 36-42.

Copyright

Copyright: © 2022 Evrim Suna Arikan Söylemez., et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.




Metrics

Acceptance rate35%
Acceptance to publication20-30 days

Indexed In




News and Events


  • Certification for Review
    Acta Scientific certifies the Editors/reviewers for their review done towards the assigned articles of the respective journals.
  • Submission Timeline for Upcoming Issue
    The last date for submission of articles for regular Issues is December 25, 2024.
  • Publication Certificate
    Authors will be issued a "Publication Certificate" as a mark of appreciation for publishing their work.
  • Best Article of the Issue
    The Editors will elect one Best Article after each issue release. The authors of this article will be provided with a certificate of "Best Article of the Issue"

Contact US