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Endometriosis is a common gynecological condition with unclear pathogenesis. Although a dysregulated lncRNA expression profile has been speculated, very few studies have addressed this hypothesis. We determined the differential lncRNA and mRNA expression patterns between endometriosis and control tissues, and between eutopic and normal endometrium in the proliferative phase, using RNA sequencing. The potential targets of lncRNA were predicted on the basis of cis and trans action, and lncRNAs were functionally annotated in relation to their co-expressed mRNAs. Dysregulated lncRNAs and mRNAs were screened relative to the biological features of endometriosis, and the five filtered lncRNAs were validated using qRT-PCR. A total of 9924 novel lncRNA transcripts were identified, and 86 lncRNAs and 1228 mRNAs were differentially expressed between the endometriosis and control groups. GO and KEGG pathway analysis showed that the differentially expressed lncRNAs were enriched in the biological processes and signaling pathways involved in endometriosis. A coding-noncoding gene (CNC) co-expression network was constructed using the dysregulated lncRNAs and their co-expressed mRNAs to simulate the complex intergenic interactions. This study is the first to use sequencing technology to elucidate the differentially lncRNA expression profiles of eutopic and normal endometrium in the proliferative phase of endometriosis. The dysregulated lncRNAs can potentially be novel diagnostic biomarkers and therapeutic targets of endometriosis.

To compare the patients’ outcomes of Asherman syndrome who underwent uterine adhesiolysis in luteal phase or follicular phase. A retrospective cohort study. A tertiary hospital in China. Four hundred sixty-four women suffered intrauterine adhesion who underwent monopolar adhesiolysis from March 2014 to March 2017 were analyzed. One hundred seventy-eight patients underwent operations in follicular phase (OFP) and 286 underwent operations in luteal phase (OLP). Hormone therapy was accompanied with an intrauterine device and a second-look hysteroscopy was performed postoperatively. Endometrial thickness in women was analyzed by a transvaginal 3-dimensional ultrasound examination. Re-adhesion was confirmed by a second-look hysteroscopy 3 months after hysteroscopic adhesiolysis. Pregnancy rate was acquired by questionnaires 3 months after a second-look hysteroscopy. OLP has advantages with thicker luteal endometrium (P = .001), higher pregnancy rates (P

G protein-coupled estrogen receptor 1 (GPER-1, formerly known as GPR30) has been proposed as the receptor for estrogen-induced, growth of leiomyomas though its precise mechanisms of action are not clear. We obtained leiomyoma cells (LC) and normal smooth muscle cells from 28 women (n = 28, median age 38 years, median parity 1.0). We incubated them with 17-β estradiol (E(2)), after blocking, or upregulating, expression of GPER-1 with ICI182,780 (a GPER-1 agonist) and siGPR30, respectively. We evaluated the role of GPER-1 in the mitogen-activated protein kinase (MAPK) signaling pathway using Western blot analysis. We studied cell proliferation with 3-(4,5-dimethylthiazol-2-yl)2,5-diphenyl tetrazolium bromide, and, mitotic activity with phosphohistone H3 (PPH3) expression in leiomyoma, and, matched, normal, smooth muscle tissues using standard immunohistochemistry. Downregulation of GPER-1 expression with siGPR30 partially attenuated the E(2)-activated MAPK signaling pathway (p 0.01). Upregulation of GPER-1 with ICI182,780 enhanced the E(2)-activated MAPK signaling pathway (p 0.01). ICI182,780 enhanced E(2)-induced proliferation of LC (p 0.01), while knock down of the GPER-1 gene with GPER-1 small interfering RNA partially inhibited E(2)-induced cell proliferation (p 0.01). There were no significant differences in PPH3 expression between LCs and normal smooth muscle tissues (p 0.05). Neither ICI182,780 nor siGPR30 increased mitosis in LCs (p 0.05). Our results indicate that GPER-1 mediates proliferation of estrogen-induced, LC by activating the MAPK pathway, and, not by promoting mitosis.

Objective To evaluate the effects of prophylactic uterine artery embolization (UAE) on second-trimester induced abortions in patients with placenta previa. Methods The present study was a retrospective review of second-trimester induced abortions in the presence of placenta previa that conducted between January 1, 2008, and October 31, 2017, at a university hospital in Hangzhou, China. Pregnancy outcomes including intraoperative blood loss, transfusion, dilatation and evacuation, hysterotomy delivery, and hysterectomy were compared between patients with and without prophylactic UAE. Results There were 54 patients included in the study. In patients with partial placenta previa (n=15), the volume of intraoperative blood loss and the frequency of dilatation and evacuation were not significantly different between the UAE and non-UAE groups (P>0.05). No patient had a transfusion, hysterotomy delivery, or hysterectomy. Among patients with complete placenta previa (n=39), the volumes of intraoperative blood loss (P=0.014) and transfusion (P=0.046) were significantly lower in the UAE group compared with the non-UAE group. The rates of dilatation and evacuation, and hysterotomy delivery did not differ between the groups (P>0.05), but were numerically higher in the non-UAE group. No patient was treated with hysterectomy. Conclusion Prophylactic UAE before a second-trimester induced abortion had significant advantages in women with complete placenta previa, but it did not improve the pregnancy outcome in patients with partial placenta previa. Chinese clinical trial registry ChiCTR-OPC-14005334.

To investigate the effect of aquaporin 5(AQP5) on proliferation and migration of ectopic endometrial epithelial cells.AQP5 shRNA interference fragments were designed and transfected into ectopic endometrial epithelial cells stably by lentivirus technology. Fluorescence quantitative RT-PCR and Western blotting were used to detect the AQP5 mRNA and protein expression, respectively. The cell proliferation and migration were determined by using MTT method and Transwell system, respectively. Levels of phosphorylated AKT(p-AKT) and total AKT were examined by Western blotting. The nude mice model of endometriosis was constructed and the endometrial cell nodule formation was observed.AQP5 shRNA transfection inhibited cell proliferation and migration compared with control group (both P0.05). The activation of AKT in AQP5 shRNA transfected cells was lower than that in control cells (P0.01). Compared to control group, the endometrial cells nodule formation was suppressed in mice inoculated with AQP5 shRNA-silencing ectopic endometrial epithelial cells.Down-regulation of AQP5 expression can suppress the proliferation and migration of ectopic endometrial epithelial cells and endometrial cell nodule formation in nude mice, in which AKT pathway may be involved.

Objective To investigate the expression of aquaporin (AQP) in eutopic and ectopic endometrial tissues from women with endometriomas. Design Controlled laboratory research. Setting Hospital-based unit for gynecology and obstetrics and research laboratories. Patient(s) Premenopausal women undergoing laparoscopy for endometriomas. Intervention(s) Endometrial biopsy samples obtained from 70 women with endometriomas. Main Outcome Measure(s) Semiquantitative analysis by immunohistochemistry. Result(s) Aquaporins 2, 5, and 8 were mainly located in luminal and glandular epithelia. The frequency of positive immunostaining for aquaporins 2, 5, and 8 decreased in ectopic compared with eutopic endometria. Aquaporins 2, 5, and 8 were found at a low frequency in the endometria in early proliferative phases but at a higher frequency in late proliferative and secretory phases. There were no significant differences in the menstrual cycle of the proliferative phase and secretory phase in the two groups. Conclusion(s) Aquaporins 2, 5, and 8 were expressed with greater frequency in eutopic endometrial cells than inectopic endometrial cells, suggesting that eutopic endometrial cells have stronger migration activity than ectopic endometrial cells in women with endometriosis.

Aquaporin 5 (AQP5) participates in the migration of endometrial cells. Elucidation of the molecular mechanisms associated with AQP5-mediated, migration of endometrial cells may contribute to a better understanding of endometriosis. Our objectives included identifying the estrogen-response element (ERE) in the promoter region of the AQP5 gene, and, investigating the effects of AQP5 on ectopic implantation of endometrial cells. Luciferase reporter assays and electrophoretic mobility shift assay (EMSA) identified the ERE-like motif in the promoter region of the AQP5 gene. After blocking and up-regulating estradiol (E2) levels, we analysed the expression of AQP5 in endometrial stromal (ES) cells. After blocking E2 /or phosphatidylinositol 3 kinase(PI3K), we analysed the role of AQP5 in signaling pathways. We constructed an AQP5, shRNA, lentiviral vector to knock out the AQP5 gene in ES cells. After knock-out of the AQP5 gene, we studied the role of AQP5 in cell invasion, proliferation, and the formation of ectopic endometrial implants in female mice. We identified an estrogen-response element in the promoter region of the AQP5 gene. Estradiol (E2) increased AQP5 expression in a dose-dependent fashion, that was blocked by ICI182,780(an estrogen receptor inhibitor). E2 activated PI3K /protein kinase B(AKT) pathway (PI3K/AKT), that, in turn, increased AQP5 expression. LY294002(PI3K inhibitor) attenuated estrogen-enhanced, AQP5 expression. Knock-out of the AQP5 gene with AQP5 shRNA lentiviral vector significantly inhibited E2-enhanced invasion, proliferation of ES cells and formation of ectopic implants. Estrogen induces AQP5 expression by activating ERE in the promoter region of the AQP5gene, activates the PI3K/AKT pathway, and, promotes endometrial cell invasion and proliferation. These results provide new insights into some of the mechanisms that may underpin the development of deposits of ectopic endometrium.

Aquaporin (AQP)-dependent cell migration has broad implications in angiogenesis, tumor metastasis, wound healing, glial scarring and other events requiring cell movement. There are 13 isoforms of AQP (0–12) that have been identified in mammals. It is unclear whether AQP5 plays a role in the development of endometrial cancer. We recently demonstrated that ovarian steroids may affect the expression of AQP5 in the female genital tract. In this study, we considered whether AQP5 may affect cell migration in Ishikawa cells, an adenocarcinoma cell line derived from the endometrium. The results showed that the downregulation of AQP5 results in reduced Ishikawa cell migration. The estrogen (E2) receptor in the promoter of AQP5 mediated the regulation of AQP5 expression in the normal endometrium and endometrial cancer. By contrast, the upregulation of AQP5 by E2 increased cell migration, invasion and adhesion through increased annexin-2, which is responsible for F-actin remodeling and rearrangement. E2 regulates Ishikawa cell migration by regulating the AQP5 expression.

Hypoxic pulmonary hypertension is a life-threatening emergency if untreated. Consistent pulmonary hypertension also leads to arteries and ventricular remodeling. The clinical therapeutic strategy for pulmonary hypertension and the corresponding remodeling mainly interacts with NO, angiotensin II (Ang II) and elevated endothelin (ET) targets. In the present study, we evaluated the effects of polydatin on hypoxia-induced pulmonary hypertension. It was observed that polydatin attenuated hypoxic pulmonary hypertension, reversed remodeling, and regulated NO, Ang II, ET contents in the serum and lung samples. However, forced activation of PKC signaling by its selective activator thymeleatoxin (THX) could abate the effects of polydatain. These results suggest that polydatin might be a promising candidate for hypoxic pulmonary treatment through interaction with PKC mechanisms.

► Cytogenetic analysis performed on peripheral blood showed a similar abnormal chromosomal complement in tumor tissue. ► Thus, mutation of an X chromosome appears to be confined to the neoplasm. ► This anomaly has not been previously described in aggressive angiomyxoma.

To investigate the DNA genome and RNA expression in 5-flurocytosine-resistant strains of Candida albicans from vaginal candidasis.Sixteen strains of Candida albicans were selected from clinically diagnosed revul-vaginal candidasis. Eight 5-flurocytosine-sensitive isolates and 8 resistant isolates were examined by France Media FUNGUS sensitive test. DNA genome was detected with random amplification polymorph DNA. RNA expression was detected with random amplification polymorph RNA method.There were no distinct differences between 5-flurocytosine-sensitive and resistant Candida albicans in DNA genome, while RNA expression showed significant differences between 5-flurocytosine-resistant and sensitive strains.Clinical 5-flurocytosine-resistant strains of Candida albicans from revul-vaginal candidasis may be related to phenotype changes.