References of "Kinugasa-Taniguchi, Yukiko"
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See detailThe effect of tumor-associated protein RCAS1 gene silencing on blood pressure and urinary protein excretion in pregnant mouse: a pilot study.
Tskitishvili, Ekaterine ULg; Nakamura, Hitomi; Kinugasa-Taniguchi, Yukiko et al

in American Journal of Obstetrics and Gynecology (2010), 203(4), 3646-36412

OBJECTIVE: The level of tumor-associated receptor-binding cancer antigen that is expressed on SiSo cells (RCAS1) is decreased significantly in preeclamptic pregnancies. We hypothesized that RCAS1 protein ... [more ▼]

OBJECTIVE: The level of tumor-associated receptor-binding cancer antigen that is expressed on SiSo cells (RCAS1) is decreased significantly in preeclamptic pregnancies. We hypothesized that RCAS1 protein gene silencing might affect blood pressure and proteinuria in pregnant mice. STUDY DESIGN: On postcoital day 7.5, pregnant imprinting control region mice were subjected to the transfer of small interfering RNA (siRNA) against RCAS1 protein into the uterine cavity with the use of a hemagglutinating virus Japan envelope. Scramble siRNA was used as a negative control. Blood pressure and urine albumin/creatinine measurements were performed. The effect of the transferred siRNA was examined in uterine samples on postcoital day 8.5 with the use of Western blotting and immunohistochemistry analyses. RESULTS: In the RCAS1 siRNA group, blood pressure significantly raised on postcoital days 9.5, 10.5, 11.5, and 15.5, whereas urine albumin/creatinine ratio was significantly increased on postcoital day 9.5 CONCLUSION: Our results suggest the importance of RCAS1 protein in the pathophysiologic condition of preeclampsia. [less ▲]

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See detailMaternal Blood Serum and Plasma Human Tumor-Associated Antigen RCAS1 During the Course of Uncomplicated Pregnancies: A Prospective Study.
Tskitishvili, Ekaterine ULg; Sharentuya, Namuxila; Tsubouchi, Hiroaki et al

in American Journal of Reproductive Immunology (2010), 64(3), 218-24

Citation Tskitishvili E, Sharentuya N, Tsubouchi H, Kinugasa-Taniguchi Y, Kanagawa T, Shimoya K, Tomimatsu T, Kimura T. Maternal blood serum and plasma human tumor-associated antigen RCAS1 during the ... [more ▼]

Citation Tskitishvili E, Sharentuya N, Tsubouchi H, Kinugasa-Taniguchi Y, Kanagawa T, Shimoya K, Tomimatsu T, Kimura T. Maternal blood serum and plasma human tumor-associated antigen RCAS1 during the course of uncomplicated pregnancies: a prospective study. Am J Reprod Immunol 2010; 64: 218-224 Problem We aimed to investigate the expression of the tumor-associated RCAS1 protein in maternal blood of uncomplicated pregnancies. Method of study Maternal blood was obtained from women with uncomplicated pregnancies (N = 43) at 11-13, 20-22, 32-34, 37-38 weeks of gestation, and immediately after delivery. Serum RCAS1 concentration was studied by ELISA, and plasma mRNA was subjected to real-time (RT)-PCR. Results Serum RCAS1 protein concentration was significantly up-regulated at 11-13 and 20-22 weeks than that at 32-34 weeks and after delivery. RCAS1 mRNA level was significantly increased at 11-13 weeks than that at 37-38 weeks. A significant positive correlation was defined between RCAS1 serum concentration at 11-13 weeks and gestational age at delivery and that between plasma RCAS1 mRNA levels at 37-38 weeks and umbilical cord blood base excess. A significant negative correlation was found between RCAS1 serum concentration at 37-38 weeks and umbilical cord blood pH at delivery. Conclusions RCAS1 protein might have importance in the development of uncomplicated pregnancies and for the prediction of pregnancy outcome. [less ▲]

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See detailTemporal and spatial expression of tumor-associated antigen RCAS1 in pregnant mouse uterus.
Tskitishvili, Ekaterine ULg; Nakamura, Hitomi; Kinugasa-Taniguchi, Yukiko et al

in American Journal of Reproductive Immunology (2010), 63(2), 137-43

PROBLEM: The tumor-associated antigen RCAS1 (receptor-binding cancer antigen expressed on SiSo cells) is considered to play a role in the inhibition of maternal immune response during pregnancy, and ... [more ▼]

PROBLEM: The tumor-associated antigen RCAS1 (receptor-binding cancer antigen expressed on SiSo cells) is considered to play a role in the inhibition of maternal immune response during pregnancy, and participates in the initiation of labor and placental detachment. The aim of our study was to investigate the expression of RCAS1 protein in the uteri of normal pregnant mice. METHOD: of study Uteri with fetuses were collected from pregnant ICR mice on days 1.5, 3.5, 5.5, 7.5, and 9.5 p.c., and uterine and placental tissues were obtained separately on days 11.5, 13.5, 15.5, and 17.5 p.c. Samples were examined using real-time (RT)-PCR, Western blotting, and immunohistochemical analyses. RESULTS: In normal pregnant mice, RCAS1 protein mRNA was significantly increased on day 7.5 p.c. Antigen localization was detected in the placenta, decidua, and fetus. CONCLUSION: The results of this study suggest the importance of day 7.5 p.c. for RCAS1 protein expression in connection with placentation as a possible target for future in vivo studies. [less ▲]

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See detailNicotine suppresses interleukin-6 production from vascular endothelial cells: a possible therapeutic role of nicotine for preeclampsia.
Sharentuya, Namuxila; Tomimatsu, Takuji; Mimura, Kazuya et al

in Reproductive Sciences (2010), 17(6), 556-63

Normal pregnancy is the controlled state of inflammation and this systemic inflammatory response is reported to be more intense in preeclampsia. The current study tested the hypothesis that maternal serum ... [more ▼]

Normal pregnancy is the controlled state of inflammation and this systemic inflammatory response is reported to be more intense in preeclampsia. The current study tested the hypothesis that maternal serum stimulates interleukin 6 (IL-6) production from endothelial cells and that nicotine inhibits these effects. Human umbilical vein endothelial cells (HUVECs) were incubated with or without 0.5% serum from healthy pregnant women at term (n = 5) and treated with or without nicotine (10(-9) to 10(-6) mol/L) in the presence of 0.5% serum. Cell survival was determined by colorimetric assay. Interleukin 6 concentration and nuclear transcription factor kappa B (NF-kB) activities were determined by enzyme-linked immunosorbent assay (ELISA)-based method. Interleukin 6 production by endothelial cells was significantly stimulated in the presence of maternal serum. Nicotine significantly preserved cell survival and suppressed IL-6 production from endothelial cells. Nicotine also significantly inhibited NF-kB activation in endothelial cells. Nicotine inhibited inflammatory reaction through NF-kB suppression in vitro model of maternal vascular endothelium, and this effect may be one of the explanations for the reduced risk of preeclampsia in smokers. [less ▲]

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See detailNicotine restores endothelial dysfunction caused by excess sFlt1 and sEng in an in vitro model of preeclamptic vascular endothelium: a possible therapeutic role of nicotinic acetylcholine receptor (nAChR) agonists for preeclampsia.
Mimura, Kazuya; Tomimatsu, Takuji; Sharentuya, Namuxila et al

in American Journal of Obstetrics and Gynecology (2010), 202(5), 4641-6

OBJECTIVE: In this study we tested the hypothesis that nicotine restores proangiogenic functions to endothelial cells pretreated with soluble fms-like tyrosine kinase 1 and/or soluble endoglin. STUDY ... [more ▼]

OBJECTIVE: In this study we tested the hypothesis that nicotine restores proangiogenic functions to endothelial cells pretreated with soluble fms-like tyrosine kinase 1 and/or soluble endoglin. STUDY DESIGN: Wound healing assay and tube formation assay were performed using human umbilical vein endothelial cells treated with nicotine (10(-9) to 10(-6) M), and with various combinations of soluble fms-like tyrosine kinase 1 (100 ng/mL), soluble endoglin (100 ng/mL), and nicotine (10(-7) M). Enzyme-linked immunosorbent assay was performed to measure vascular endothelial growth factor, placental growth factor, and transforming growth factor-beta1 concentrations in the conditioned media treated with nicotine (10(-9) to 10(-6) M). RESULTS: Nicotine significantly facilitated endothelial migration and tube formation. By contrast, soluble fms-like tyrosine kinase 1 and/or soluble endoglin suppressed these endothelial functions. Nicotine restored these soluble fms-like tyrosine kinase 1 and/or soluble endoglin-reduced endothelial functions. Placental growth factor, but not transforming growth factor-beta1, production was significantly stimulated by the presence of nicotine. Vascular endothelial growth factor was undetectable. CONCLUSION: Our results suggest a possible mechanism for the protective effects of cigarette smoking against preeclampsia, thus proposing a therapeutic potential of nicotine or other nicotinic acetylcholine receptor agonists for preeclampsia. [less ▲]

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See detailOxidative stress-induced S100B protein from placenta and amnion affects soluble Endoglin release from endothelial cells.
Tskitishvili, Ekaterine ULg; Sharentuya, Namuxila; Temma-Asano, Kumiko et al

in Molecular Human Reproduction (2010), 16(3), 188-99

Oxidative stress with elevated intracellular Ca(2+) concentration as well as endothelial dysfunction is a component of pre-eclampsia. Our aim was to investigate the oxidative stress-dependent expression ... [more ▼]

Oxidative stress with elevated intracellular Ca(2+) concentration as well as endothelial dysfunction is a component of pre-eclampsia. Our aim was to investigate the oxidative stress-dependent expression of Endoglin and Ca(2+)-binding S100B protein from villous and amniotic tissue cultures, and to assess sEng expression from S100B protein-stimulated endothelial cells. We initially examined Endoglin and Hydroxy-nonenal-(HNE)-modified proteins in the placentas and amnion obtained from women with pre-eclampsia (n = 8), and healthy controls (n = 8) by immunohistochemistry. To examine oxidative stress and the S100B protein effect on sEng expression from endothelial cells, normal villous and amniotic tissue cultures were stimulated by 4-HNE, sodium fluoride and xanthine/xanthine oxidase, whereas human umbilical vein endothelial cell cultures were treated with S100B protein in a dose- and time-dependent manner at 37 degrees C in an environment of 95% air and 5% of CO(2). Culture supernatants were assessed using ELISA. Cell viability was determined using MTS assay. The concentrations of sEng and S100B protein were significantly increased in the villous and amniotic tissue culture supernatants under oxidative stress. S100B protein-stimulated endothelial cells released sEng into conditioned media with a significantly higher expression levels at a concentration of 200 pM-20 nM S100B by 2 h, whereas treated with 200 nM of S100B endothelial cells significantly expressed sEng by 12 h and stimulated the cell proliferation by the same period of time. Our findings show that oxidative stress affects sEng and S100B protein expression from villous and amniotic tissues, and picomolar and low nanomolar concentrations of S100B protein significantly up-regulate sEng release from endothelial cells leading to endothelial dysfunction. [less ▲]

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See detailNicotine suppresses interleukin-6 production from vascular endothelial cells
Tomimatsu, Takuji; Sharentuya, Namuxila; Mimura, Kazuya et al

Poster (2009)

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See detailNicotine restores endothelial dysfunction caused by excess sFLT1 and sEng in in vitro model pf preeclamptic vascular endothelium
Mimura, Kazuya; Tomimatsu, Takuji; Sharentuya, Namuxila et al

Poster (2009)

Detailed reference viewed: 9 (3 ULg)