Decidualization modulates a signal transduction system via protease-activated receptor-1 in endometrial stromal cells

2018 ◽  
Vol 80 (5) ◽  
pp. e13036
Author(s):  
Kaori Goto ◽  
Yasushi Kawano ◽  
Takafumi Utsunomiya ◽  
Hisashi Narahara
Keyword(s):  
Signal Transduction ◽  
Stromal Cells ◽  
Signal Transduction System ◽  
Endometrial Stromal Cells ◽  
Protease Activated Receptor 1

The signal transduction pathways via protease activated receptor-1 (PAR-1) in human decidual stromal cells

2015 ◽  
Vol 112 ◽  
pp. 128
Author(s):  
Kaori Goto ◽  
Fumiko Kawabe ◽  
Yasushi Kawano ◽  
Takafumi Utsunomiya ◽  
Hisashi Narahara
Keyword(s):  
Signal Transduction ◽  
Stromal Cells ◽  
Signal Transduction Pathways ◽  
Protease Activated Receptor 1

Progesterone-independent induction of decidualization of endometrial stromal cells of patients with and without endometriosis

2015 ◽  
Vol 75 (07) ◽  
Author(s):  
J Thomczik ◽  
I Beyer ◽  
DM Baston-Büst ◽  
SJ Böddeker ◽  
G Wennemuth ◽  
...  
Keyword(s):  
Stromal Cells ◽  
Endometrial Stromal Cells

Regulation of TIMP-1, -2 and -3 in human endometrial stromal cells during decidualization and under the influence of hCG

2006 ◽  
Vol 114 (S 1) ◽  
Author(s):  
S Krenzer ◽  
H Fluhr ◽  
M Deperschmidt ◽  
M Zwirner ◽  
D Wallwiener ◽  
...  
Keyword(s):  
Stromal Cells ◽  
Endometrial Stromal Cells

ÜBER DIE BILDUNG VON ENDOMETRIALEN KÖRNCHENZELLEN BEI KASTRATINNEN UNTER HORMONEINFLUSS

1960 ◽  
Vol XXXIII (II) ◽  
pp. 261-276 ◽  
Author(s):  
G. Hellweg ◽  
J. Ferin ◽  
K. G. Ober
Keyword(s):  
Hormone Therapy ◽  
Stromal Cells ◽  
Sex Hormone ◽  
Substitution Therapy ◽  
Secretory Phase ◽  
Hormone Substitution ◽  
Endometrial Stromal Cells ◽  
Endometrial Stroma ◽  
K Cells

ABSTRACT 65 endometrial biopsies from castrated women who had received either natural or artificial sex hormone therapy were studied microscopically. Attention was paid to various histologic criteria, especially to the number of endometrial granulocytes (»K« cells, KZ). The following was obtained: The »K« cells are completely absent when no hormone substitution therapy is given. They were also lacking when the castrated patients were treated only with oestrogens, even if the dose given was ten-times that found in women during the reproductive ages. In contrast, the »K« cells developed from the endometrial stromal cells only under influence of progesterone, usually appearing first 8–10 days after the administration of the gestagen. The »K« cells were demonstrable in the number corresponding to a normal secretory phase only then, when the oestrogen-progesterone dosage ratio had induced a fully-developed secretory change, as measured by the usual histologic criteria. With an overdosage of oestrogen the »K« cells were either absent or were very sparse. Contrarily, an overdosage of progesterone had no influence on their number. The development of endometrial glands does not always entirely parallel that of the stroma in castrated patients following hormone therapy. A more exact indicator for the proper dose for the production of a secretory phase by hormone therapy seems to be the number of »K« cells in the endometrial stroma.

Inhibition of TMEM16A impedes embryo implantation and decidualization in mice

Reproduction ◽  
2018 ◽  
Author(s):  
Qianrong Qi ◽  
Yifan Yang ◽  
Kailin Wu ◽  
Qingzhen Xie
Keyword(s):  
Progesterone Receptor ◽  
Stromal Cells ◽  
Embryo Implantation ◽  
Mouse Uterus ◽  
Endometrial Stromal Cells ◽  
Uterine Endometrium ◽  
Molecule Inhibitor ◽  
Pathway Inhibition ◽  
And Function ◽  
Reproductive Processes

Recent studies revealed that TMEM16A is involved in several reproductive processes, including ovarian estrogen secretion and ovulation, sperm motility and acrosome reaction, fertilization, and myometrium contraction. However, little is known about the expression and function of TMEM16A in embryo implantation and decidualization. In this study, we focused on the expression and regulation of TMEM16A in mouse uterus during early pregnancy. We found that TMEM16A is up-regulated in uterine endometrium in response to embryo implantation and decidualization. Progesterone treatment could induce TMEM16A expression in endometrial stromal cells through progesterone receptor/c-Myc pathway, which is blocked by progesterone receptor antagonist or the inhibitor of c-Myc signaling pathway. Inhibition of TMEM16A by small molecule inhibitor (T16Ainh-A01) resulted in impaired embryo implantation and decidualization in mice. Treatment with either specific siRNA of Tmem16a or T16Ainh-A01 inhibited the decidualization and proliferation of mouse endometrial stromal cells. In conclusion, our results revealed that TMEM16A is involved in embryo implantation and decidualization in mice, compromised function of TMEM16A may lead to impaired embryo implantation and decidualization.

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