Persistent Stimulation of Sex-related Hormones in the Uterus is Associated with Differences in the Igf/Akt Signaling Pathway and Uterine Damage

被引:0
作者
Oh, Min Jee [1 ,2 ]
Choi, Yun Dong [3 ]
Kim, Sang Hwan [1 ,2 ]
机构
[1] Hankyong Natl Univ, Sch Anim Life Convergence Sci, 327 Jungang Ro, Ansung 17579, Gyeonggi Do, South Korea
[2] Hankyong Natl Univ, Inst Appl Humanimal Sci, 327 Jungang Ro, Ansung 17579, Gyeonggi Do, South Korea
[3] Seoul Hoseo Occupat Training Coll, Seoul 07583, South Korea
关键词
Difference; Endocrine disruption; IGF signal; Sex; Testosterone; Uterine health; POLYCYSTIC-OVARY-SYNDROME; ANDROGEN EXCESS; HB-EGF; MECHANISMS; WOMEN;
D O I
10.18805/IJAR.BF-1886
中图分类号
S8 [畜牧、 动物医学、狩猎、蚕、蜂];
学科分类号
0905 ;
摘要
Background: The health of the female endometrium is determined by a delicate network of hormones and signaling genes. Our study analyzed the effects of continuous excess of major sex-related hormones on insulin-like growth factor/protein kinase B (IGF/Akt) signaling on the functional and morphological changes of the endometrium. Methods: After estrus synchronization of six mice, human chorionic gonadotropin (hCG), pregnant mare serum gonadotrophin (PMSG), progesterone (P4) andtestosterone (TES) were overstimulated andthe differences in IGF/Akt signal expression were analyzed using an immunoassay method. Result: The results of this study showed that the morphological changes of the uterus in the hCG and P4 treatment groups had very similar patterns and the expression of genes belonging to the IGF/Akt signaling pathway affected maturation of the endometrium uterine gland and induced expression of pregnancy-associated plasma protein to increase the maturation rate of the uterus. However, the TES treatment group showed increased uterine apoptotic factors and inhibited endometrial development. Therefore, based on the results of this study, hormonal stimulation can have different effects on the functional maturation and morphological development of the uterus andrepeated hormonal excess processes can be predicted through IGF/Akt signaling.
引用
收藏
页码:574 / 580
页数:7
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