Background: MiR-198 has been considered as an inhibitor of cell proliferation, invasion, migration and a promoter of apoptosis in most cancer cells, while its effect on non-cancer cells is poorly understood. Methods: The effect of miR-198 transfection on HaCaT cell proliferation was firstly detected using Cell Count Kit-8 and the cell cycle progression was analyzed by flow cytometry. Using bioinformatics analyses and luciferase assay, a new target of miR-198 was searched and identified. Then, the effect of the new target gene of miR-198 on cell proliferation and cell cycle was also detected. Results: Here we showed that miR-198 directly bound to the 3′-UTR of CCND2 mRNA, which was a key regulator in cell cycle progression. Overexpressed miR-198 repressed CCND2 expression at mRNA and protein levels and subsequently led to cell proliferation inhibition and cell cycle arrest in the G1 phase. Transfection ofSiCCND2 in HaCaT cells showed similar inhibitory effects on cell proliferation and cell cycle progression. Conclusion: In conclusion, we have identified that miR-198 inhibited HaCaT cell proliferation by directly targeting CCND2.

Preimplantation genetic diagnosis (PGD) is becoming a widely-accepted technique during in vitro fertilization (IVF). However, a disadvantage of PGD is the invasive biopsy methods used to sample embryonic cells or polar bodies. Recent studies have found that genetic material can be detected in blastocoel fluid (BF) and culture medium. In our study, BF and trophectoderm (TE) cells were simultaneously collected from the same donated human blastula. To generate enough DNA for analysis, we used multiple displacement amplification (MDA) based whole genome amplification (WGA). MDA-WGA samples were probed with primers designed to identify spinal muscular atrophy (SMA) and phenylpropionate ketoneuria (PKU), plus the Y chromosome sex-determining region (SRY). This demonstrated that DNA fragments were present in each of the TE and BF samples (7/7). The positive PCR amplification rates for SMA, PKU, SRY and β-actin in BF were 42.9% (3/7), 60% (3/5), 42.9% (3/7) and 71.4% (5/7) respectively, but the positive rate of amplification with TE samples was 100% (7/7), 100% (7/7), 71.43% (5/7) and 100% (7/7). After sequencing, identical alleles were found in matched BF and TE samples. In summary, BF-DNA could be detected using MDA-WGA and PCR, and sequences in PCR positive samples were identical in matched BF-DNA and TE samples.

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Uterine peristalsis is essential for gamete transport and embryo implantation. It shares the characteristics of spontaneity, rhythmicity, and directivity with gastrointestinal peristalsis.Telocytes, the "interstitial Cajal-like cells" outside the digestive canal, are also located in the uterus and may act as pacemakers. To investigate the possible origin and regulatory mechanism of periodic uterine peristalsis in the human menstrual cycle, telocytes in the myometrium were studied to determine the effect of estradiol on T-type calcium channel regulation. In this study, biopsies of the human myometrium were obtained for cell culture, and double-labeling immunofluorescence screening was used to identify telocytes and T-type calcium channel expression. Intracellular calcium signal measurements and patch-clamp recordings were used to investigate the role of T-type calcium channels in regulating calcium currents with or without estradiol. Our study demonstrates that telocytes exist in the human uterus and express T-type calcium channels. The intracellular Ca 2+ fluorescence intensity marked by Fluo-4AM was dramatically decreased by NNC 55-0396, a highly selective T-type calcium channel blocker, but enhanced by estradiol. T-type calcium current amplitude increased in telocytes incubated with estradiol in a dose-dependent manner compared to the control group. In conclusion, our study demonstrated that telocytes exist in the human myometrium, expressing T-type calcium channels and estradiol-enhanced T-type calcium currents, which may be a reasonable explanation for the origin of uterine peristalsis. The role of telocytes in the human uterus as pacemakers and message transfer stations in uterine peristalsis may be worth further investigation.