Sepideh Mousazadeh - Ph.D., Department of Tissue Engineering and Regenerative Medicine, Faculty of Advanced Technologiesin Medicine, Iran University of Medical Sciences, Tehran, Iran- Department of Genetics, Reproductive Biomedicine Research Center, Royan Institute for Reprod
Azadeh Ghaheri - Ph.D.,Department of Epidemiology and Reproductive Health, Reproductive Epidemiology ResearchCenter, Royan Institute for Reproductive Biomedicine, ACECR, Tehran, Iran
Maryam Shahhoseini - Ph.D., Department of Genetics, Reproductive Biomedicine Research Center, Royan Institute for Reproductive Biomedicine, ACECR, Tehran, Iran- Department of Epidemiology and Reproductive Health, Reproductive Epidemiology Research Center, Royan Institute for
Reza Aflatoonian - Department of Endocrinology and Female Infertility, Reproductive Biomedicine Research Center, Royan Institute for Reproductive Biomedicine, ACECR, Tehran, Iran

Background: Endometriosis are defined as a progesterone-resistance disease. Twoprogesterone receptor (PR) isoforms, namely PR-A and PR-B, mediate the specialeffects of progesterone. One of the most effective polymorphism in the promoter regionof PGR is the +331G/A.Objective: The differential expression level of PR isoforms due to +331G/A polymorphismmay be able to influence the function of progesterone and reduce thesusceptibility of endometriosis.Materials and Methods: This analytic, case-control study was carried out at RoyanInstitute, Tehran, Iran. Whole-blood samples were collected from 98 infertile womenundergoing laparoscopy for endometriosis and 102 healthy fertile women. After DNAextraction, genotype frequencies were determined by polymerase chain reactionrestrictionfragment length polymorphism. Then, RNA was extracted from the selectedeutopic tissue samples of endometriosis patients. Analysis of PR-A and PR-B mRNAexpressions were performed using Real-time polymerase chain reaction.Results: The frequency distribution of GG, GA genotypes in +331G/A polymorphismwas 98.04%, 1.96% in the patients and 97.96%, 2.04% in the control groups, respectively(p = 0.968). Although our data did not show any significant association with +331G/Ain the patient and control groups, we were able to demonstrate significantly higherexpression level of PR-B and no significant lower expression level of PR-A isoforms inpatients by favoring GA to GG genotypes (p = 0.017, p = 0.731, respectively).Conclusion: Our findings show that patients with GA genotypes had a higherexpression level of PR-B compared to patients with GG genotypes.

Endometriosis, Progesterone receptor A, Progesterone receptor B, rs10895068