Correction to: miR-205-5p inhibits human endometriosis progression by targeting ANGPT2 in endometrial stromal cells.

An amendment to this paper has been published and can be accessed via the original article.

miR-205-5p inhibits human endometriosis progression by targeting ANGPT2 in endometrial stromal cells.

BACKGROUND: miRNA expression profiles in ectopic endometrium (EC) serving as pathophysiologic genetic fingerprints contribute to determining endometriosis progression; however, the underlying molecular mechanisms remain unknown. METHODS: miRNA microarray analysis was used to determine the expression profiling of EC fresh tissues. qRT-PCR was performed to screen miR-205-5p expression in EC tissues. The roles of miR-205-5p and its candidate target gene, angiopoietin-2 (ANGPT2), in endometriosis progression were confirmed on the basis of both in vitro and in vivo systems. miR-205-5p and ANGPT2 expression were measured by in situ hybridization and immunochemistry, and their clinical significance was statistically analysed. RESULTS: miR-205-5p was screened as a novel suppressor of endometriosis through primary ectopic endometrial stromal cell migration, invasion, and apoptosis assay in vitro, along with endometrial-like xenograft growth and apoptosis in vivo. In addition, ANGPT2 was identified as a direct target of miR-205-5p through bioinformatic target prediction and luciferase reporter assay. Re-expression and knockdown of ANGPT2 could respectively rescue and simulate the effects induced by miR-205-5p. Importantly, the miR-205-5p-ANGPT2 axis was found to activate the ERK/AKT pathway in endometriosis. Finally, miR-205-5p and ANGPT2 expression were closely correlated with the endometriosis severity. CONCLUSION: The newly identified miR-205-5p-ANGPT2-AKT/ERK axis illustrates the molecular mechanism of endometriosis progression and may represent a novel diagnostic biomarker and therapeutic target for disease treatment.

[Effect of GnRHa therapy following conservative laparoscopic surgery for endometriosis on clinical pregnant rate in patients with endometriosis-associated infertility].

OBJECTIVE: To investigate the impact of conservative laparoscopic surgery for endometriosis with postoperative gonadotropin-releasing hormone agonist (GnRHa) therapy on the pregnancy outcomes in patients with endometriosis-associated infertility. METHODS: The clinical data were collected from the patients with endometriosis-associated infertility undergoing conservative laparoscopic surgery in our department between January, 2011 and December, 2016. The patients were divided into laparoscopic surgery only group (without any other treatments) and postoperative GnRha therapy group, and the pregnancy outcomes were compared between the two groups at different time points during the follow-up. RESULTS: In cases with moderate or severe endometriosis, laparoscopic surgery with postoperative GnRha therapy was associated with a significantly higher clinical pregnancy rate than laparoscopic surgery alone (P<0.05). In patients receiving postoperative GnRha therapy, the accumulative pregnancy rates at 6, 12, 24 and 36 months after discontinuation of GnRha therapy were significantly higher than those in patients receiving laparoscopic surgery alone. The pregnancy rate following IVF-ET cycles was significantly higher than the spontaneous pregnancy rate in patients receiving conservative laparoscopic surgery alone (P<0.05), while such a difference was not found in patients with postoperative GnRHa therapy (P>0.05). CONCLUSIONS: GnRHa therapy after conservative laparoscopic surgery can significantly increase the clinical pregnancy rate in infertile 6 months women with moderate or severe endometriosis but not in mild cases. Within 6 months following laparoscopic surgery or following discontinuation of GnRHa therapy is the optimal time window for pregnancy, and a longer time from therapy discontinuation is associated with a lower possibility of spontaneous pregnancy.