Introduction: Studies have shown that long non-coding RNAs (lncRNA) are aberrantly expressed in polycystic ovarian syndrome (PCOS) ovaries and may have a role in PCOS development. In this study, the role and therapeutic implications of lncRNA H19 were investigated in PCOS ovaries and granulosa cells. Material and methods: qRT-PCR was used for expression analysis. Cell Counting Kit 8 (CCK-8) assay was used for cell viability and acridine orange/ ethidium bromide (AO/EB) and Annexin V/propidium iodide staining was used to detect apoptosis. All transfections were carried out with Lipofectamine 2000 reagent. Western blot analysis was used for protein expression analysis. Results: The expression of lncRNA H19 was remarkably upregulated in the PCOS ovarian tissues as well as the granulosa cells. Suppression of lncRNA H19 expression caused the inhibition of KGN granulosa cell proliferation due to the triggering of apoptosis. Bioinformatic analysis revealed the presence of the GAS binding site for STAT3 in the promoter of lncRNA H19. Silencing of STAT3 suppressed the expression of lncRNA H19 in KGN cells and also halted their growth by triggering apoptosis. Co-transfect experiments revealed that STAT3 and lncRNA H19 silencing cause inhibition of KGN growth synergistically. Conclusions: lncRNA H19 regulates the growth of ovarian granulosa cells and might prove to be a therapeutic target for management of PCOS.

The present study aimed to investigate whether premature rupture of the fetal membrane, combined with subclinical chorioamnionitis, affects pregnancy outcomes. In addition, the association between premature rupture of the fetal membrane (PROM) and the levels of matrix metalloproteinase-2 (MMP-2), an inactive proenzyme that can be activated by other factors or signals in humans, was examined. In total, 80 pregnant patients with PROM were classified into the experimental and control groups, according to their final placental pathological diagnosis results. The 40 patients in the experimental group suffered from subclinical chorioamnionitis, while the 40 patients in the control group exhibited no lesions of the placenta or fetal membrane. Tissue samples were collected and the total protein and mRNA were extracted for western blot and quantitative polymerase chain reaction analyses. ELISA was performed in order to detect the levels of MMP-2 in the serum of the two groups of patients. The rates of cesarean section, puerperal infection, postpartum hemorrhage, preterm incidence, placenta accreta, residual placental blood and stillbirth were all significantly higher in the experimental group compared with the control group. In addition, the mRNA and protein expression levels of MMP-2 were reduced in the experimental group compared with the control group. ELISA results indicated that the serum MMP-2 concentrations were also reduced in the patients with PROM. Therefore, the present study demonstrated that the PROM, combined with subclinical chorioamnionitis, significantly affected pregnancy outcomes and was associated with reduced levels of MMP-2.

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