Maebashi-shi, Japan
Maebashi-shi, Japan

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Igarashi S.,Gunma University | Igarashi T.,Teikyo University | Abe Y.,Gunma University | Liang S.-G.,Teikyo University | And 2 more authors.
Journal of Endometriosis and Pelvic Pain Disorders | Year: 2013

Background: Among several theories explaining the pathogenesis of endometriosis, Sampson's theory seems to be the most reliable and popular. However, this theory does have some problems. First, the onset of endometriosis is not as common as retrograde menstruation. Second, the surface of the peritoneum is capable of preventing the adhesion of foreign bodies such as endometrial cells. Regarding the first problem, several studies on immunosurveillance have been reported. The second problems has not yet been clarified, Therefore we investigated the problem in the present report. Methods: Levels of CD44 and tenascin in both menstrual and peripheral blood were assayed in 19 healthy volunteer women in the first experiment. In the second experiment, the effects of tenascin on the activity of MMP-9 were investigated, because the invasive ability of endometriotic cells is known to be due to MMP activity. Results: CD44 and tenascin concentrations were significantly higher in menstrual blood than in peripheral blood. Since CD44 is a specific hyaluronic acid receptor, CD44 in menstrual blood was demonstrated to be a specific matchmaker of adhesion between the endometrial cells and the peritoneal surface. Tenascin in menstrual blood and endometriotic cells up-regulated MMP activity and promoted the invasive action of endometriotic cells. Conclusion: The present study clarified that adhesion of endometrial cells in menstrual blood on adhesion- preventive peritoneal surface was achieved by a mediator, CD44, in menstrual blood and that the ability of endometriotic cells to invade, induced by MMP, was achieved through up-regulation of MMP activity by the mediator tenascin. © 2013 Wichtig Editore.

Yokota Y.,Yokota Maternity Hospital | Yokota H.,Yokota Maternity Hospital | Yokota M.,Yokota Maternity Hospital | Araki Y.,Maebashi Institute of Technology
Reproductive Medicine and Biology | Year: 2015

Purpose: To evaluate the effect of long-term caffeine administration on murine sperm and subsequent in vitro fertilization (IVF). Methods: Male mice were injected with various doses (0, 0.2 and 1.0 mg/mouse/day) of caffeine for 1 month. After sperm collection, the IVF rate and embryo development to the blastocyst stage were evaluated. Results: The mean body weight significantly decreased in the 1.0 mg/day treatment group compared to the control group (P < 0.01). Testicular weight and histological features did not differ, and total blood testosterone was no different in spite of the difference between 0.2 and 1.0 mg/day of caffeine. The IVF rate differed significantly between the control group [100/105 (95.2 %)] and 0.2 mg/day group [106/121 (87.6 %)] (P < 0.05). Furthermore, blastocyst formation was significantly and dose-dependently lower with higher caffeine levels: control group: 85/100 (85.0 %); 0.2 mg/day group: 84/106 (79.2 %) (P < 0.05); 1.0 mg/day group: 64/102 (62.7 %) (P < 0.001). Conclusions: Caffeine treatment affected body weight of male mice. However, testicular weight, histological features and total blood testosterone concentration were not statistically different. In addition, following IVF using sperm from these mice, blastocyst formation decreased in a dose-dependent manner. These findings suggest that embryo development from oocytes fertilized with sperm from caffeine-administered male mice is negatively affected. © 2015, Japan Society for Reproductive Medicine.

Yokota H.,Yokota Maternity Hospital | Yokota Y.,Yokota Maternity Hospital | Yokota M.,Yokota Maternity Hospital | Araki Y.,Maebashi Institute of Technology
Reproductive Medicine and Biology | Year: 2013

Purpose: To evaluate the effect of long-term caffeine administration to mice on in vitro fertilization (IVF) of oocytes. Methods: Mice were injected with different dosages (0, 0.1, and 1.0 mg/mouse/converted day) of caffeine for one month. Subsequently, the fertilization rate and embryo development to blastocyst stage were evaluated in IVF using oocytes from the mice. Results: The retrieved average oocyte rate was significantly lower (27.4) in mice injected with 1.0 mg caffeine than in the control group (36.5; P < 0.05); the fertilization rate was significantly different between the 0 mg (317/401; 79.1 %) and 1.0 mg group (199/301; 66.1 %) (P < 0.05). At 96 h after insemination, the blastocyst formation rate was significantly decreased in the 1.0 mg group (94/199; 47.2 %) compared with the control (0 mg) group (237/317; 74.8 %) and 0.1 mg group (226/323; 70 %) (P < 0.05). When 1.0 mg caffeine was administered for two weeks, embryo development was significantly impacted. Conclusions: Our findings suggest that caffeine administration negatively impacts oocytogenesis and embryonic development after IVF. © 2013 Japan Society for Reproductive Medicine.

Abe Y.,Gunma University | Komatsubara M.,Yokota Maternity Hospital | Saito M.,Fujioka General Hospital | Toda M.,Cancer Institute | And 5 more authors.
Journal of Endocrinological Investigation | Year: 2013

Background: Accumulating evidence supports the idea of activin A as a modulator of inflammation. In human pregnancy, elevated activin A concentrations in amniotic fluid are reported in women with intra-amniotic infection and inflammation- induced pre-term birth. Aim: To test the hypothesis that activin A was involved in the pathophysiology of amnionitis, we evaluated the effects of tumor necrosis factor-α and lipopolysaccharide on activin A production in human amniotic epithelial cells, and the effects of activin A on the expression of collagen mRNA in amniotic mesenchymal cells. Materials and methods: Amniotic membranes were obtained from patients without systemic disease, signs of premature delivery or fetal complications, during elective cesarean sections at term. Amniotic epithelial cells and mesenchymal cells were separately obtained by enzymatic digestion and cultured. Activin A was measured by enzyme-linked immunosorbent assay and collagen mRNA levels were assessed by quantitative PCR. Results: Amniotic epithelial cells produced activin A in a cell density- and time-dependent manner. Tumor necrosis factor-α enhanced activin A production in a time-dependent (48-120 h) and dose-dependent (10-300 ng/ml) manner in amniotic epithelial cells. Lipopolysaccharide also stimulated activin A production, but the effect was less prominent. In amniotic mesenchymal cells, the effect of activin A on the expression of type I and type III collagen mRNA was suppressive. Conclusions: Tumor necrosis factor-α and lipopolysaccharide stimulated activin A production in amniotic epithelial cells, and activin A modulated expression of collagen mRNA in amniotic mesenchymal cells. These results support the idea that activin A is involved in the pathophysiology of amnionitis. © 2013, Editrice Kurtis.

Abe Y.,Gunma University | Marukawa R.,Kuki General Hospital | Tsuru N.,Miyazaki Prefectural Nobeoka Hospital | Sato M.,Yokota Maternity Hospital | And 4 more authors.
International Journal of Endocrinology | Year: 2013

Activin A is involved in inflammation. The present study was performed to clarify if lipopolysaccharide, a component of Gram-negative bacteria, stimulates activin A secretion from human amniotic epithelial cells and to determine if activin A plays a role in amnionitis. Fetal membranes were obtained during elective cesarean sections performed in full-term pregnancies of patients without systemic disease, signs of premature delivery, or fetal complications. Amniotic epithelial cells were isolated by trypsinization. The activin A concentrations in the culture media were measured by enzyme-linked immunosorbent assay, and cell proliferation was assessed by 5-bromo-2′-deoxyuridine incorporation. Amniotic epithelial cells secreted activin A in a cell density-dependent manner, and lipopolysaccharide (10 g/mL) enhanced the secretion at each cell density. Lipopolysaccharide (10-50 g/mL) also stimulated activin A secretion in a dose-dependent manner. Contrary to the effect of activin A secretion, lipopolysaccharide inhibited cell proliferation in amniotic epithelial cells. The present study suggests that lipopolysaccharide stimulation of activin A secretion may be a mechanism in the pathogenesis of amnionitis. © 2013 Yumiko Abe et al.

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