Reduced expression of Il10, Stat3, Hoxa10, and Itgb3 in the embryo implantation site of rat model with prenatal androgen‐induced polycystic ovary syndrome

Author:

Changaei Mostafa1,Javidan Moslem1,Ramezani Tehrani Fahimeh2,Mosaffa Nariman3,Noroozzadeh Mahsa2,Hosseinzadeh Ramin1,Rajaei Samira1ORCID

Affiliation:

1. Department of Immunology School of Medicine Tehran University of Medical Sciences Tehran Iran

2. Reproductive Endocrinology Research Center Research Institute for Endocrine Sciences Shahid Beheshti University of Medical Sciences Tehran Iran

3. Department of Immunology School of Medicine Shahid Beheshti University of Medical Sciences Tehran Iran

Abstract

AbstractAimsImpaired implantation due to the reduced endometrial receptivity considers an etiology for infertility in polycystic ovary syndrome (PCOS). In this context, we aimed to compare the expression of interleukin 10 (Il10), homeobox A10 (Hoxa10), signal transducer and activator of transcription 3 (Stat3), and β3‐integrin (Itgb3) in the embryo implantation site of a prenatally‐androgenized rat model of PCOS before and during gestation.Materials and MethodsPCOS rat model was created by the injection of testosterone prenatally. The uterine tissues were collected before pregnancy (day 0) and on days 0.5, 4.5, 5.5, and 8.5 of gestation in the PCOS rat model and controls (n = 6; each group). RNA was extracted from the uterine samples and reverse transcribed to cDNA. Expression levels of Il10, Stat3, Hoxa10, and Itgb3 were measured using SYBR Green real‐time RT‐PCR and compared between the two groups.FindingsPCOS rats showed decreased expression levels of the Il10 on day 8.5 compared to control rats. The mRNA levels of Hoxa10, Itgb3, and Stat3 were significantly decreased in the PCOS group on day 0 as well as on days 0.5, 4.5, 5.5, and 8.5 for Hoxa10, Itgb3, and Stat3.SignificanceThe decreased gene expression of Il10, Hoxa10, Stat3, and Itgb3 in the PCOS rat model indicates the importance of the Il10 signaling axis as one of the possible disrupted mechanisms of endometrial receptivity in PCOS.

Publisher

Wiley

Subject

Obstetrics and Gynecology,Reproductive Medicine,Immunology,Immunology and Allergy,Obstetrics and Gynecology,Immunology

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