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Cellular oscillators in the uterus play critical roles in the gestation processes of mammals through entraining of the clock proteins to numerous downstream genes, including growth/differentiation factor ( Gdf) 10 and Gdf15. The expression of Gdf10 and Gdf15 is significantly increased in the uterus during decidualization, but the mechanism underlying the regulation of Gdf gene expression in the uterus is poorly understood. Here, we focused on the function of the cellular oscillators in the expression of Gdf family by using uterine endometrial stromal cells ( UESCs) isolated from pregnant Per2- dLuc transgenic rats. A significant decline of Per2- dLuc bioluminescence activity was induced in in vitro decidualized UESCs, and concomitantly the expression of canonical clock genes was downregulated. Conversely, the expression of Gdf10 and Gdf15 of the Gdf was upregulated. In UESCs transfected with Bmal1-specific si RNA, in which Rev-erbα expression was downregulated, Gdf10 and Gdf15 were upregulated. However, Gdf5, Gdf7, and Gdf11 were not significantly affected by Bmal1 silencing. The expression of Gdf10 and Gdf15 was enhanced after treatment with a REV- ERB α antagonist in the presence or absence of progesterone. Chromatin immunoprecipitation- PCR analysis revealed the inhibitory effect of REV- ERB α on the expression of Gdf10 and Gdf15 in UESCs by recognizing their gene promoters. Collectively, our findings indicate that the attenuation of REV- ERB α leads to an upregulation of Gdf10 and Gdf15 in decidual cells, in which cellular oscillators are impaired. Our results provide novel evidence regarding the functions of cellular oscillators regulating the expression of downstream genes during the differentiation of UESCs. [ABSTRACT FROM AUTHOR]

This study aimed to develop an in vitro model for the analysis of the bovine endometrium. Immunofluorescent staining revealed that the hetero-spheroids and the cultured explants showed almost similar structure in the localization of bovine endometrial epithelial cells and endometrial stromal cells, except the glandular-like structure of the epithelial cells inside the explants. Gelatin zymography revealed that the hetero-spheroids did not express matrix metalloproteinases ( MMPs) after 4 days of culture, but strong MMP expressions were observed in the cultured explants until 7 days of culture. Additionally, expression of progesterone receptor ( PR), estrogen receptor alpha ( ERα), type I interferon receptor 1 (IFNAR1) and 2 (IFNAR2) messenger RNA was observed both in the homo- and hetero-spheroids. The expression of oxytocin receptor ( OTR) mRNA in E2 and E2+ P4 (1,3,5(10)-Estratrien-3, 17β-diol + 4-Pregnen-3, 20-dinone) treated groups were significantly ( P < 0.05) higher than that of the control group of spheroids. In case of cultured explants, the expression of PR and OTR mRNA were significantly ( P < 0.05) higher in E2 treated groups compared to the control groups. Hepatocyte growth factor ( HGF) mRNA expression was also higher in P4 treated groups at 10 days in culture ( P < 0.05). In a nutshell, the in vitro model developed in this study for the analysis of the endometrium may provide a new platform for extensive research on bovine endometrial function. [ABSTRACT FROM AUTHOR]

BACKGROUND The present study was conducted to evaluate the developmental toxicity in the endometrium and placenta due to GW501516 administration by gavage to pregnant rats. METHODS GW501516 was orally administered repeatedly to pregnant rats from gestation day ( GD) 6 to 17 at a dose of 0, 30, and 100 mg/kg/day. In next study, GW501516 was also orally administered to pregnant rats on GD 7, 8, 9, 10, or 11 at a single dose of 275 or 350 mg/kg. In these studies, caesarean section was performed to examine the pregnancy outcome on GD21. Additionally, GW501516 was orally administered to pregnant rats on GD 10 at a single dose of 275 mg/kg. Placentae were subjected for temporal histological examinations on GD 11, 13, 15, or 17. RESULTS Placental malformation was induced by repeated administration of GW501516 at a dose of 100 mg/kg/day. Single oral administration of GW501516 at a dose of 275 and/or 350 mg/kg on GD 8, 9, 10, or 11 induced placental malformation, whereas GW501516 administered on GD 10 was the most effective for increasing placental malformation. Histopathologically, single oral administration of GW501516 on GD 10 induced cystic degeneration associated with cellular lysis of glycogen cells started from GD 15 in the basal zone. CONCLUSIONS High frequency of placental malformation was observed by the administration of GW501516. From GD 8 to 11, especially GD 10, is more sensitive period to induce the placental malformation. [ABSTRACT FROM AUTHOR]

The article discusses research on the possible effects of ectopic expression of the human telomerase reverse transcriptase (hTERT) on the proliferation of chicken feather keratinocyte stem cells (FKSCs). Researchers isolated native FKSCs from feather follicles of neonatal chicken wings and then cloned them with the limited dilution method. Results of the study detected ectopic expression of hTERT-epidermal growth factor receptor (EGFP) in FKSCs transduced by retrovirus which could lead to understanding human telomerase activity.

Nitric oxide (NO) is synthesized by three NO synthases, designated as NOS-1, NOS-2, and NOS-3, with distinct features and localization. Nitric oxide and the reactive oxygen species generated from NO react with a wide variety of biomolecules such as DNA, transcription factors, enzymes, cytokines, and membrane receptors in NO synthesized cells and nearby cells to mediate a variety of biological functions. Nitric oxide synthase-2 and NOS-3 are expressed in the ovary during folliculogenesis and luteinization. Nitric oxide functions as an important modulator for folliculogenesis and atresia, steroidogenesis, prostaglandin biosynthesis, ovulation, luteolysis, and oocyte maturation. Nitric oxide synthase-3 is also localized in the porcine oocytes of the primordial follicles as well as in large follicles. It has been proved that NO is involved in intracellular signaling for oocyte growth and maturation at the pre-ovulatory stage. [ABSTRACT FROM AUTHOR]