Published date: Jan 09 2023

Journal Title: International Journal of Reproductive BioMedicine

Issue title: International Journal of Reproductive BioMedicine (IJRM): Volume 20, Issue No. 12

Pages: 1007–1012

DOI: 10.18502/ijrm.v20i12.12561

Zhima AkhavansalesDepartment of Immunology, Faculty of Medicine, International Campus, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.

Alimohammad MosadeghmehrjardiDepartment of Traditional Pharmacy, Faculty of Traditional Medicine, Tehran University of Medical Sciences, Tehran, Iran.

Hamid Reza AshrafzadehAbortion Research Center, Yazd Reproductive Sciences Institute, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.

Shadnaz Fakhteh YavariDepartment of Tissue Engineering and Applied Cell Science, School of Advanced Technologies in Medicine, Shahid Beheshti University of Medical Science, Tehran, Iran.

Mohammad Taher TahooriDepartment of Immunology, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.

Morteza Bitaraf SaniAnimal Science Research Department, Yazd Agricultural and Natural Resources Research and Education Center, Agricultural Research, Education & Extension Organization (AREEO), Yazd, Iran.

Mahnaz MohammadiAbortion Research Center, Yazd Reproductive Sciences Institute, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.

Fateme MontazeriAbortion Research Center, Yazd Reproductive Sciences Institute, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.

Nasrin Ghaseminghasemi479@gmail.comAbortion Research Center, Yazd Reproductive Sciences Institute, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.

Background: Premature ovarian failure (POF), is menopause occurring before the age of 40, affecting 1-3% of women worldwide. The risk of POF increases with altered immunological parameters such as FAS and FASL genes, which play a fundamental role in embryogenesis and cellular homeostasis.

Objective: The study aimed to investigate the potential role of FAS and FASL genes in POF pathogenesis.

Materials and Methods: In this case-control study, the polymorphisms of FAS-670A/G and FASLIVS2nt_124A/G apoptotic genes were analyzed in 51 Iranian women suffering from POF, and 61 healthy controls. Isolation of DNA was done using the salting-out method, and genotypic analysis was performed for all the subjects using the polymerase chain reaction-restriction fragment length polymorphism method.

Results: Our results revealed that homozygous FAS-670A/A and G/G, and heterozygous FAS-670A/G are not significantly different between cases and controls (p = 0.99). Also, in different genotyping models of FASIVS2nt_124, polymorphisms were not related to POF risk (p = 0.23).

Conclusion: There is no statistical association between these polymorphisms and POF risk in women referred to genetic counseling clinics.

Key words: FAS, FASL, Polymorphism, Premature ovarian failure.

[1] Christin-Maitre S, Givony M, Albarel F, Bachelot A, Bidet M, Blanc JV, et al. Position statement on the diagnosis and management of premature/primary ovarian insufficiency (except Turner Syndrome). Ann Endocrinol 2021; 82: 555– 571.

[2] Direkvand-Moghadam A, Sayehmiri K, Delpisheh A, Direkvand-Moghadam A. The global trend of infertility: An original review and meta-analysis. Int J Epidemiol Res 2014; 1: 35–43.

[3] Arora P, Polson DW. Diagnosis and management of premature ovarian failure. Obstet Gynecol 2011; 13: 67–72.

[4] Zhang Ch. The roles of different stem cells in premature ovarian failure. Curr Stem Cell Res Ther 2020; 15: 473–481.

[5] Igboeli P, El Andaloussi A, Sheikh U, Takala H, ElSharoud A, McHugh A, et al. Intraovarian injection of autologous human mesenchymal stem cells increases estrogen production and reduces menopausal symptoms in women with premature ovarian failure: Two case reports and a review of the literature. J Med Case Rep 2020; 14: 1–11.

[6] Sari S. Analysis of androgen receptor gene mutations in female with infertility. Scientific Information Database 2017; 19: 1–7.

[7] Pargianas M, Salta S, Apostolopoulou K, Lazaros L, Kyrgiou M, Tinelli A, et al. Pathways involved in premature ovarian failure: A systematic review of experimental studies. Curr Pharm Des 2020; 26: 2087–2095.

[8] Parsa E, Hoseini SM, Namayandeh SM, Akhavansales Zh, Sheikhha MH. Investigating the rate of different ovarian response in in vitro fertilization cycles based on estrogen receptor beta+ 1730 polymorphism: A cross-sectional study. Int J Reprod BioMed 2020; 18: 509–516.

[9] Sbracia M, Valeri C, Antonini G, Biagiotti G, Pacchiarotti A, Pacchiarotti A. Fas and fas-ligand in eutopic and ectopic endometrium of women with endometriosis: The possible immune privilege of ectopic endometrium. Reprod Sci 2016; 23: 81–86.

[10] Liu Z, Li F, Xue J, Wang M, Lai S, Bao H, et al. Esculentoside A rescues granulosa cell apoptosis and folliculogenesis in mice with premature ovarian failure. Aging (Albany NY) 2020; 12: 16951–16962.

[11] Harada T, Taniguchi F, Izawa M, Ohama Y, Takenaka Y, Tagashira Y, et al. Apoptosis and endometriosis. Front Biosci 2007; 12: 3140–3151.

[12] Lettau M, Paulsen M, Schmidt H, Janssen O. Insights into the molecular regulation of FasL (CD178) biology. Eur J Cell Biol 2011; 90: 456–466.

[13] Eslami MM, Rezaei R, Abdollahi S, Davari A, Ahmadvand M. FAS-670A > G gene polymorphism and the risk of allograft rejection after organ transplantation: A systematic review and meta-analysis. Blood Res 2021; 56: 17–25.

[14] Sibley K, Rollinson S, Allan JM, Smith AG, Law GR, Roddam PL, et al. Functional FAS promoter polymorphisms are associated with increased risk of acute myeloid leukemia. Cancer Res 2003; 63: 4327–4330.

[15] Akhavan Sales Zh, Tahoori MT, Sheikhha MH, Seifati SM, Bitaraf Sani M. Identification of a FAS/FASL haplotype associated with endometriosis in Iranian patients. Gynecol Endocrinol 2020; 36: 261–264.

[16] Jafari M, Nasiri MR, Sanaei R, Anoosheh S, Farnia P, Sepanjnia A, et al. The NRAMP1, VDR, TNF-α, ICAM1, TLR2 and TLR4 gene polymorphisms in Iranian patients with pulmonary tuberculosis: A case-control study. Infect Genet Evol 2016; 39: 92–98.

[17] Mohammadzadeh A, Pourfathollah AA, Sahraian MA, Behmanesh M, Daneshmandi S, Moeinfar Z, et al. Evaluation of apoptosis-related genes: FAS (CD94), FASL (CD178) and TRAIL polymorphisms in Iranian multiple sclerosis patients. J Neurol Sci 2012; 312: 166–169.

[18] Zhang Z, Wang LE, Sturgis EM, El-Naggar AK, Hong WK, Amos CI, et al. Polymorphisms of FAS and FAS ligand genes involved in the death pathway and risk and progression of squamous cell carcinoma of the head and neck. Clin Cancer Res 2006; 12: 5596–5602.

[19] Agic A, Djalali S, Diedrich K, Hornung D. Apoptosis in endometriosis. Gynecol Obstet Invest 2009; 68: 217–223.

[20] D’Arcy MS. Cell death: A review of the major forms of apoptosis, necrosis and autophagy. Cell Biol Int 2019; 43: 582–592.

[21] Slot KA, Voorendt M, de Boer-Brouwer M, van Vugt HH, Teerds KJ. Estrous cycle dependent changes in expression and distribution of Fas, Fas ligand, Bcl-2, Bax, and pro-and active caspase-3 in the rat ovary. J Endocrinol 2006; 188: 179–192.

[22] Mohammadzadeh A, Pourfathollah AA, Tahoori MT, Daneshmandi S, Langroudi L, Akhlaghi M. Evaluation of apoptosis-related gene FAS (CD95) and FASL (CD178) polymorphisms in Iranian rheumatoid arthritis patients. Rheumatol Int 2012; 32: 2833–2836.