WNT7A (rs104893832) polymorphism increases the risk of recurrent spontaneous abortion in Iranian women

Main Article Content

Manouchehr Mazdapour
Mahmood Dehghani Ashkezari
Seyed Morteza Seifati

Abstract

BACKGROUND
Recurrent spontaneous abortion is defined as the occurrence of three or more clinical miscarriages in one woman. Several factors, including genetics and environmental factors, are involved in this kind of infertility, in which WNT7A (rs104893832) polymorphism plays a major role. The aim of the present study was to determine the association between a common polymorphism of WNT7A (rs104893832) with recurrent spontaneous abortion in females.

METHODS
In the present case-control study, the WNT7A (rs104893832) polymorphism was investigated in 70 women with recurrent spontaneous abortion as cases and 100 women with at least one child and no history of infertility or abortion as controls. Polymerase chain reaction- restriction fragment length polymorphism (PCR-RFLP) was used to investigate the WNT7A (rs104893832) polymorphism in both case and control groups. The data were subsequently analyzed using the chi-square and logistic regression tests by SPSS software (version 18.0).

RESULTS
A significant association was found between the WNT7A (rs104893832) polymorphism and recurrent spontaneous abortion (OR=25.00, 95% CI=5.52-157.09; p<0.0001). Our finding showed that G allele frequency in women with recurrent spontaneous abortion was significantly different compared to the control group. (OR=6.42, 95% CI=2.82-15.16; p<0.0001).Therefore, genetic variation in WNT7A (rs104893832) polymorphism may play a role in recurrent spontaneous abortion.

Conclusion
This study revealed that WNT7A (rs104893832) polymorphism increased the risk of recurrent spontaneous abortion. Knowledge of these mutations and polymorphisms can provide an insight into the prognosis for individual patients. Therefore, further studies are necessary to establish the association of WNT7A (rs104893832) polymorphism with recurrent spontaneous abortion in a larger population.

Article Details

How to Cite
Mazdapour, M., Ashkezari, M. D., & Seifati, S. M. (2018). WNT7A (rs104893832) polymorphism increases the risk of recurrent spontaneous abortion in Iranian women. Universa Medicina, 37(3), 167–172. https://doi.org/10.18051/UnivMed.2018.v37.167-172
Section
Original Articles

References

Doubilet PM, Benson CB, Bourne T, et al. Diagnostic criteria for nonviable pregnancy early in the first trimester. N Engl J Med 2013;369:1443-51. doi: 10.1056/NEJMra1302417.

Larsen EC, Christiansen OB, Kolte AM, et al. New insights into mechanisms behind miscarriage. BMC Med 2013;11:154-9. doi: 10.1186/17417015.11.154.

Kaur R, Gupta K. Endocrine dysfunction and recurrent spontaneous abortion: an overview. Int J Appl Basic Med Res 2016;6:79-83. doi: 10.4103/2229-516X.179024.

Nigro G, Mazzocco M, Mattia E, et al. Role of infections in recurrent spontaneous abortion. J Matern Fetal Neonatal Med 2011;24:983-89. doi: 10.3109/14767058.2010.547963.

Wong LF, Porter T, Scott JR. Immunotherapy for recurrent miscarriage. Cochrane Database of Systematic Reviews 2014;10:112-8. doi: 10.1002/14651858.CD000112.pub3.

Battinelli EM, Marshall A, Jean M. The role of thrombophilia in pregnancy. Thrombosis 2013;3:487-501. doi: 10.1155/2013/516420.

Lassi Z, Imam A, Dean SV, et al. Preconception care: caffeine, smoking, alcohol, drugs and other environmental chemical/radiation exposure. Reprod Health 2014;26:154-60. doi: 10.1186/1742475511.

Hyde KJ, Schust DJ. Genetic considerations in recurrent pregnancy loss. Cold Spring Harb Perspect Med 2015;5:a023119. doi: 10.1101/cshperspect.a023119.

He H, Li T, Yin D, et al. HOXA10 expression is decreased by testosterone in luteinized granulosa cells in vitro. Mol Med Rep 2012;6:51-6. doi: 10.3892/mmr.2012.875.

Quinonez SC, Innis JW. Human HOX gene disorders. Mol Genet Metab 2014;111:4-15. doi: 10.1016/10012.

May L, Kuningas M, Bodegom D, et al. Genetic variation in pentraxin (PTX) 3 gene associates with PTX3 production and fertility in women. Biol Reprod 2010;82:299-304. doi: 10.1095/biolreprod.109.079111.

Tiwari M, Prasad S, Pandey NA, et al. Nitric oxide signaling during meiotic cell cycle regulation in mammalian oocytes. Front Biosci 2017;9:307-318. doi:10.2741/s489.

Garavelli L, Wischmeijer A, Rosato S, et al. Al-Awadi-Raas-Rothschild (limb/pelvis/uterus--hypoplasia/aplasia) syndrome and WNT7A mutations: genetic homogeneity and nosological delineation. Am J Med Genet 2011;155:332-6. doi: 10.1002/ajmg.a.33793.

Sondereggera S, Pollheimerb J, Knoflerb M. Wnt Signalling in implantation, decidualisation and placental differentiation – review. Placenta 2010;31:839–47. doi: 10.1016/j.placenta.2010.07.011.

Vainio S, Heikkila M, Kispert A, et al. Female development in mammals is regulated by Wnt-4 signalling. Nature 1999;397:405-409.

Fan X, Krieg S, Hwang J, et al. Dynamic regulation of Wnt7a expression in the primate endometrium: Implications for postmenstrual regeneration and secretory transformation. Endocrinol 2012:153:1063-1069. doi: 10.1210/en.2011-1826.

Tepekoy F, Akkoyunlu G, Demir R. The role of Wnt signaling members in the uterus and embryo during pre-implantation and implantation. J Assist Reprod Genet 2015;32:337-348 doi: 10.1007/s10815-014-0409-7

Dunlap KA, Filant J, Hayashi K, et al. Postnatal deletion of Wnt7a inhibits uterine gland morphogenesis and compromises adult fertility in mice. Biol Reprod 2011;85:386–96. doi: 10.1095/biolreprod.111.091769.

van Amerongen R, Nusse R. Towards an integrated view of Wnt signaling in development. Development 2009;136:3205-14. doi: 10.1242/dev.033910.

Gilbert SF. Developmental biology. 9th ed. Sunderland: Mass Sinauer Associates;2010.