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C Tadokoro

Publications and source records attributed to C Tadokoro.

10 recordsLinked to original sources
PubMed1998

Effects of imipramine and sertraline on protein kinase activity in rat frontal cortex.

Three-week administration of sertraline or imipramine to rats (10 mg/kg, intraperitoneally, twice a day) increased ex vivo cyclic AMP-dependent protein kinase activity in the soluble but not in the particulate fraction of the frontal cortex. However, cyclic AMP-dependent protein kinase activity was not affected in either fraction of the parietotemporal cortex and hippocampus. Neither antidepressant altered protein kinase C activity in the soluble and particulate fractions or Ca2+/calmodulin-dependent protein kinase II activity in the frontal cortex. Therefore, sertraline and imipramine both selectively enhance cyclic AMP-dependent protein kinase activity in the frontal cortex. This enhancement might be involved in their biochemical mechanisms.

1-Naphthylamine↗
PubMed1997

Behavioral stimulation without alteration of beta and 5-HT receptors and adenylate cyclase activity in rat brain after chronic sertraline administration.

Effects of chronic treatment with selective 5-HT reuptake inhibitors (SSRIs) on the monoaminergic functions have not been much investigated in compared with tricyclic antidepressants. Therefore, we compared the effects of 3-week treatment with sertraline, a potent SSRI, to those of imipramine (10 mg/kg, IP, twice a day), on monoamine receptors and adenylate cyclase (AC) activity in rat brain. Two-week treatment with both sertraline and imipramine reduced immobility in the water wheel test to the comparable extent. Sertraline treatment did not affect Kd and Bmax of [3H]CGP12177 and [3H]ketanserin bindings or cAMP, accumulation by norepinephrine, isoproternol, 5'-guanylylimidodiphosphate [Gpp(NH)p] and forskolin in the cortical membrane compared with vehicle-treated rats. On the other hand, imipramine treatment decreased Bmax of both bindings and norepinephrine- or isoproternol-stimulated cAMP accumulation. Treatment with either antidepressant induced no apparent changes in [3H]8-OH-DPAT [2-(N, N-dipropylamino)-8-hydroxy-1,2,3,4-tetrahydronaphthalene] binding in the hippocampal membrane. These results suggested that chronic treatment of sertraline induced little effect on monoamine receptors and AC activity in the brain and that the alteration of these functions may not be primarily involved in antidepressive effects of antidepressants, at least of SSRIs.

1-Naphthylamine↗
PubMed1996

8-Bromo-cAMP inhibits glucose transport activity in mouse placental cells in culture.

Glucose plays an important role in fetal development and energy metabolism. Facilitative glucose transporter-1 (GLUT1) has been found in placenta. However, little is known about GLUT1 modulation in placental cells. To examine changes in mouse placental GLUT1 levels caused by 8-bromo-cAMP, we performed 2-deoxyglucose uptake experiments, Northern blot analysis and immunoblot analysis using a primary mouse placental cell culture. Immunohistochemical analysis showed that GLUT1 was localized to the ectoplacental cone and the labyrinth zone of mouse placentas on days 7 and 11 of pregnancy respectively. Treatment of mouse placental cells with 250 mumol/l 8-bromo-cAMP resulted in a significant (P < 0.01) decrease in glucose uptake on days 2-5 of culture. The inhibitory effect of 8-bromo-cAMP on glucose uptake was concentration-dependent. Glucose uptake was also inhibited by 100 micrograms/l cholera toxin and by 0.1 mmol/l forskolin. Northern blot and immunoblot analysis revealed that both GLUT1 mRNA and protein levels were also decreased by 8-bromo-cAMP. These findings suggest that 8-bromo-cAMP inhibits glucose transport activity in mouse placental cells in culture.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1996

Localization of human placental glucose transporter 1 during pregnancy. An immunohistochemical study.

To elucidate the potential roles of glucose transporter 1 (GLUT1) in human placenta during pregnancy, we examined the localization of GLUT1 in human placenta at various stages by immunohistochemistry with an anti-GLUT1 antibody by use of both light and electron microscopy. Specific staining for GLUT1 was localized on the apical brush border and along the basal plasma membrane of the syncytiotrophoblasts. The staining at the apical side was more intense than that at the basal side during the early stages of gestation. In later gestational stages, however, the staining pattern at the apical side became blurred and the staining intensity at the basal side increased. The cytotrophoblasts, seen embedded in the basal part of the syncytiotrophoblasts, seemed to show immunoreactivity for GLUT1 along the plasma membranes at the light-microscopic level. However, immuno-electron microscopic analysis with either pre- or post-embedding methods revealed that specific staining for GLUT1 was hardly observed on the cytotrophoblasts, but the cytotrophoblasts were often surrounded by immunoreactive processes of syncytiotrophoblasts. The blood capillaries and erythrocytes in the stroma of placental villi were always immunoreactive for GLUT1 throughout pregnancy. These findings suggest that GLUT1 may play a vital role in human pregnancy.

Capillaries↗
PubMed1995

Expression and localization of glucose transporter 1 (GLUT1) in the rat oviduct: a possible supplier of glucose to embryo during early embryonic development.

The oviduct fluid mainly derived from the oviduct epithelium is reported to provide the environment necessary for embryonic development. To elucidate the origin of glucose in the oviduct fluid, we examined the expression and localization of glucose transporter 1 (GLUT1) in the rat oviduct by Northern blot analysis, immunoblot analysis and immunohistochemistry using both light and electron microscopy. Northern blot and immunoblot analyses both showed the presence of the GLUT1 mRNA and protein. Specific staining for GLUT1 was observed in the ampulla and the isthmus, but only slightly in the fimbria and the utero-tubal junction. Staining was confined to the luminal surface of the epithelial mucosa. Immunoelectron microscopic analysis revealed that GLUT1 was observed only on the surface of the microvilli in non ciliated secretory cells, but not in ciliated cells. These findings suggest that GLUT1 plays an important role in the glucose transfer from the oviduct epithelium into the lumen and in maintaining the adequate glucose concentration of the oviduct fluid for embryonic development in rat oviduct.

Animals↗
PubMed1995

Changes in epidermal growth factor receptor and the levels of its ligands during menstrual cycle in human endometrium.

We examined menstrual cycle-dependent changes in the expression of human endometrial epidermal growth factor (EGF), transforming growth factor alpha (TGF alpha), and epidermal growth factor receptor (EGFR) and their mRNA using immunoblot analysis, 125I-EGF binding, and competitive reverse transcription and polymerase chain reaction (RT-PCR). We also studied their localization in the endometrial tissue by immunohistochemistry. Endometrial samples were obtained at three stages of menstruation: the early follicular stage, which exhibits low serum estradiol (E2) and progesterone (P) levels; the late follicular stage, which exhibits high E2 and low P levels; and the luteal stage, which exhibits high E2 and P levels. Immunohistochemical examination showed that EGF, TGF alpha, and EGFR were localized to the endometrial epithelium. Immunoblot analysis revealed that endometrial EGF, TGF alpha, and EGFR levels were significantly (p < 0.01) increased at the late follicular and luteal stages compared to the early follicular stage. 125I-EGF-specific binding levels at the late follicular and luteal stages were significantly (p < 0.01) higher than at the early follicular stage, consistent with the results of immunoblot analysis. Competitive RT-PCR revealed that EGF, TGF alpha, and EGFR mRNA levels were significantly (p < 0.01) higher at the late follicular and luteal stages than at the early follicular stage. Changes in EGF, TGF alpha, and EGFR mRNA levels were consistent with changes in protein levels. These findings suggest that synthesis and expression of human endometrial EGF, TGF alpha, and EGFR vary with the stage of the menstrual cycle and that their expression in the human endometrium is associated with the increase in the serum E2 but not with the increase in P levels.

Binding, Competitive↗
PubMed1995

Increase in human placental glucose transporter-1 during pregnancy.

Glucose transporter-1 (GLUT1) has been found in high abundance in human placentas. The purpose of this study was to analyze the changes in the level of GLUT1 during pregnancy. We have analyzed the gestational changes in human placental GLUT1 by [3H]cytochalasin B binding assay, immunoblot analysis and Northern blot analysis. Levels of [3H]cytochalasin B binding to placental membrane in pregnancy at 7-10, 18-20 and 38-40 weeks were 4.2 +/- 0.47, 5.2 +/- 0.46 and 7.2 +/- 0.40 (mean +/- SEM, N = 4) mumol/kg protein, respectively. Amounts of 49-kD and 60-kD proteins detected in immunoblot analysis increased during pregnancy in parallel with [3H]cytochalasin B binding to placental membrane. The GLUT1 mRNA levels also increased during pregnancy. Immunohistochemical examination showed that GLUT1 was localized in the plasma membranes of trophoblast cells. These findings showed that the GLUT1 level increased during pregnancy in human placentas and suggest that GLUT1 may play an important role in fetal development.

Blotting, Northern↗
PubMed1994

Tumor necrosis factor-alpha (TNF-alpha) inhibits expression of mouse placental lactogen-II through TNF-alpha type-I but not type-II receptor.

The aim of this study was to determine whether TNF-alpha inhibits mPL-II secretion through TNF-RI or TNF-RII, and to investigate the gestational profile of TNF-RI and TNF-RII gene expression. The mouse trophoblast cells from day 12 pregnancy were cultured with or without agonistic polyclonal antibodies directed against the individual TNF-alpha receptors, and mPL-II secretion in the medium was assessed by RIA. Anti-TNF-RI antibody significantly inhibited the mPL-II secretion in a dose- and time-dependent manner, but anti-TNF-RII antibody did not. Moreover, the TNF-RII antibody did not influence the inhibitory effect of the TNF-RI antibody on mPL-II secretion. TNF-RI antibody inhibited the mPL-II gene expression by Northern blot analysis. Amount of the gene expression of TNF-RI in the second half of pregnancy was higher than those in the first half of pregnancy both in vitro and in vivo, although the gene expression of TNF-RII was not detectable by Northern blot analysis using poly(A)+RNA. These results suggest that TNF-RI is a main receptor for TNF-alpha in mouse placenta and that TNF-alpha may have an important role in regulating mPL-II secretion after midpregnancy.

Animals↗
PubMed1994

Involvement of autocrine mechanism of transforming growth factor-beta in the functional differentiation of pregnant mouse mammary gland.

We studied the presence and possible role of the autocrine mechanism of transforming growth factor-beta (TGF-beta) in pregnant mouse mammary gland. Northern blot analysis revealed the expression of the TGF-beta 1 gene transcript at 2.5 kb in mammary epithelial cells isolated from virgin and mid-pregnant mice. The TGF-beta activity was higher in the conditioned medium from mid-pregnant mouse mammary explants than that from virgin explants by a bioassay system using mink lung epithelial cells. A binding study using [125I]TGF-beta 1 as a ligand showed that pregnant mouse mammary epithelial cells possessed a single class of high-affinity TGF-beta 1 binding sites (Kd = 28.0 pmol/l, 1.2 x 10(4) sites per cell). These results suggested the presence of a TGF-beta autocrine mechanism in pregnant mouse mammary epithelial cells. Next, we examined the effect of TGF-beta 1 on the functional differentiation of pregnant mouse mammary gland. Transforming growth factor-beta 1 inhibited alpha-lactalbumin production in cultured mammary explants from mid-pregnant mice in a dose-dependent manner without inhibiting DNA synthesis. All these results suggest that TGF-beta may play a role in regulating the functional differentiation of mouse mammary glands during pregnancy.

Animals↗