Expression Pattern of G-Protein-Coupled Estrogen Receptor in Myometrium of Uteri with and without Adenomyosis.

Objective: To compare the expression of G-protein-coupled estrogen receptor (GPER) in the junctional zone and outer myometrium of the proliferative and secretory phases of women with and without adenomyosis.

Methods: A total of 76 women were included in this study, 42 with adenomyosis (proliferative phase, = 23; secretory phases, = 19) and 34 controls (proliferative phase, = 16; secretory phases, = 18). Protein and total RNA were extracted from the junctional zone (JZ) and outer myometrium (OM).

Human amniotic mesenchymal stromal cell transplantation improves endometrial regeneration in rodent models of intrauterine adhesions.

Background Aims: Intrauterine adhesion (IUA) is a common uterine cavity disease characterized by the unsatisfactory regeneration of damaged endometria. Recently, stem cell transplantation has been proposed to promote the recovery process. Here we investigated whether human amniotic mesenchymal stromal cells (hAMSCs), a valuable resource for transplantation therapy, could improve endometrial regeneration in rodent IUA models.

Efficacy of freeze-dried amnion graft following hysteroscopic adhesiolysis of severe intrauterine adhesions.

Objective: To evaluate the efficacy of freeze-dried amnion graft for prevention of intrauterine adhesion (IUA) reformation after hysteroscopic adhesiolysis.

Methods: A prospective randomized controlled trial was conducted among 88 women with severe IUAs who underwent hysteroscopic adhesiolysis at Beijing Obstetrics and Gynecology Hospital between July 15, 2015, and July 1, 2016. All participants had a balloon inserted into the uterine cavity for 1 week.

17β-Estradiol Induces Overproliferation in Adenomyotic Human Uterine Smooth Muscle Cells of the Junctional Zone Through Hyperactivation of the Estrogen Receptor-Enhanced RhoA/ROCK Signaling Pathway.

Adenomyosis (ADS) is a common estrogen-dependent gynecological disease with unknown etiology. Recent models favor abnormal thickening of the junctional zone (JZ) may be the causative factor in the development of ADS. RhoA, a small guanosine triphosphatase which controls multiple cellular processes, is involved in the control of cell proliferation.