Expression and function of kisspeptin during mouse decidualization.
BACKGROUND
Plasma kisspeptin levels dramatically increased during the first trimester of human pregnancy, which is similar to pregnancy specific glycoprotein-human chorionic gonadotropin. However, its particular role in the implantation and decidualization has not been fully unraveled. Here, the study was conducted to investigate the expression and function of kisspeptin in mouse uterus during early pregnancy and decidualization.


RESULTS
Quantitative PCR results demonstrated that Kiss1 and GPR54 mRNA levels showed dynamic increase in the mouse uterus during early pregnancy and artificially induced decidualization in vivo. KISS-1 and GPR54 proteins were spatiotemporally expressed in decidualizing stromal cells in intact pregnant females, as well as in pseudopregnant mice undergoing artificially induced decidualization. In the ovariectomized mouse uterus, the expression of Kiss1 mRNA was upregulated after progesterone or/and estradiol treatment. Moreover, in a stromal cell culture model, the expression of Kiss1 and GPR54 mRNA gradually rise with the progression of stromal cell decidualization, whereas the attenuated expression of Kiss1 using small interfering RNA approaches significantly blocked the progression of stromal cell decidualization.


CONCLUSIONS
our results demonstrated that Kiss1/GPR54 system was involved in promoting uterine decidualization during early pregnancy in mice.
Department of Physiology, School of Medicine, Nanchang University, Nanchang, Jiangxi, China.
Peng
P
Zhang
Department of Cell Biology, School of Medicine, Nanchang University, Nanchang, Jiangxi, China.
Min
M
Tang
Department of Physiology, School of Medicine, Nanchang University, Nanchang, Jiangxi, China; Department of Reproductive Medicine, First Affiliated Hospital of Gannan Medical University, Ganzhou, Jiangxi, China.
Ting
T
Zhong
Department of Obstetrics and Gynecology, Hospital of Jixi Province People, Nanchang, Jiangxi, China.
Yan
Y
Lin
Department of Physiology, School of Medicine, Nanchang University, Nanchang, Jiangxi, China.
Teng
T
Zong
Department of Physiology, School of Medicine, Nanchang University, Nanchang, Jiangxi, China.
Chengxue
C
Zhong
Department of Physiology, School of Medicine, Nanchang University, Nanchang, Jiangxi, China.
BaoPing
B
Zhang
Department of Physiology, School of Medicine, Nanchang University, Nanchang, Jiangxi, China.
Min
M
Ren
Department of Physiology, School of Medicine, Nanchang University, Nanchang, Jiangxi, China.
HaiBin
H
Kuang
D000818:Animals; D003656:Decidua / Q000378:metabolism*; D010064:Embryo Implantation; D005260:Female; D020869:Gene Expression Profiling; D018507:Gene Expression Regulation, Developmental; D006728:Hormones / Q000737:chemistry; D007633:Keratins / Q000378:metabolism; D059648:Kisspeptins / Q000378:metabolism*; D051379:Mice; D011247:Pregnancy; D011270:Pregnancy, Animal; D012333:RNA, Messenger / Q000378:metabolism; D043562:Receptors, G-Protein-Coupled / Q000378:metabolism; D000074502:Receptors, Kisspeptin-1; D013256:Steroids / Q000737:chemistry; D014599:Uterus / Q000196:embryology; D014746:Vimentin / Q000378:metabolism
D006728:Hormones; C491407:Kiss1 protein, mouse; C492248:Kiss1r protein, mouse; D059648:Kisspeptins; D012333:RNA, Messenger; D043562:Receptors, G-Protein-Coupled; D000074502:Receptors, Kisspeptin-1; D013256:Steroids; D014746:Vimentin; D007633:Keratins