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Biomedical subjects

O Tanizawa

Publications and source records attributed to O Tanizawa.

At least 163 records · Page 9Linked to original sources
PubMed1990

HLA expression on human ejaculated sperm.

The expression of human leukocyte antigen (HLA) on human ejaculated sperm has been investigated by using cellular binding radioimmunoassay (CB-RIA) with sperm samples purified by Percoll discontinuous gradient and monoclonal antibodies specific to the frame work of HLA molecules. The results in packed sperm obtained from ten healthy males indicated that HLA class II and its subclasses, DP, DQ, and DR, were expressed at a low level on human ejaculated sperm, while HLA class I was not detected. Furthermore, we could not detect the individual variation of HLA expression on ejaculated sperm in the cases of twenty healthy males. K562, which is B lymphoid cell line and lacks HLA class I molecules, showed detectable amounts of HLA class I molecules after exposure to interferon gamma (IFN-gamma) and/or tumor necrosis factor alpha (TNF-alpha). However, the treatment of sperm with IFN-gamma and/or TNF-alpha had no effect on the expression of HLA class I and class II molecules.

Antibodies, Monoclonal↗
PubMed1990

Gene expression of macrophage colony-stimulating factor and its receptor in human placenta and decidua.

Macrophage colony-stimulating factor (M-CSF) induces proliferation of monocyte/macrophage progenitor cells and can also activate some functions of mature cells including fetally derived placental cells. To study the role of M-CSF in the pregnant female reproductive tract, the expression of M-CSF mRNA and its receptor, c-fms proto-oncogene, in human placenta and decidua was identified. M-CSF and c-fms mRNAs, 4.7Kb and 3.9Kb respectively, were detected by Northern blotting in the early stage placenta and subsequently increased during pregnancy. These mRNAs were not detected in the nonpregnant endometrium but were strongly induced in maternal decidua with the same mRNA size as in the placenta. Northern blot hybridization on the endometrium of a pseudopregnant uterus revealed that the expression of endometrial M-CSF and c-fms mRNAs is regulated by synergistic action of female sex steroid hormones. These findings indicate that, in an autocrine and/or paracrine manner, M-CSF is deeply involved in the local proliferation and differentiation of cells at the materno-fetal interface, and support the placental immunotrophism hypothesis.

Blotting, Northern↗
PubMed1990

Dopamine inhibits the arachidonate and prolactin release stimulated by thyrotropin-releasing hormone through an islet-activating protein-sensitive GTP-binding protein in anterior pituitary cells.

Coupling of the dopamine (DA) receptor to the pathway of arachidonate (AA) through the islet-activating protein (IAP)-sensitive GTP-binding (G) protein was examined in primary cultures of anterior pituitary cells. The inhibitions by 1 microM DA of the stimulations of prolactin (PRL) release by 100 nM thyrotropin-releasing hormone and by 10 microM calcium ionophore A23187 were blocked by 100 ng/ml IAP. DA at 1 microM did not inhibit the release of [3H]-AA induced by 100 mU/ml phospholipase A2 (PLA2), but it inhibited the release of PRL induced by 100 mU/ml PLA2. This inhibition was blocked by 100 ng/ml IAP. IAP also blocked the inhibitions by DA of the releases of PRL by 5 microM AA and by 5 microM 5-hydroxyeicosatetraenoic acid. These results suggest that the DA receptor on lactotrophs is coupled to the pathway following the release of AA (lipoxygenase) through the IAP-sensitive G protein.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1990

Adenosine 3',5'-cyclic monophosphate enhances dopamine accumulation in rat hypothalamic cell culture containing dopaminergic neurons.

The regulation of dopamine accumulation in cultured rat hypothalamic cells by adenosine 3',5'-cyclic monophosphate (cAMP) was investigated in cultures of newborn rat hypothalamic cells. Both dibutyryl cAMP, (Bu)2-cAMP, and forskolin enhanced [3H]dopamine accumulation in a dose-dependent manner. cAMP also enhanced [3H]dopamine accumulation, but to a lesser degree. Neither n-butyrate nor adenosine alone enhanced [3H]dopamine accumulation. (Bu)2-cAMP had no effect on basal efflux of [3H]radioactivity. The effect of (Bu)2-cAMP appeared on day 5 of culture, reached a maximum on day 6, and then rapidly decreased. These results suggest that dopamine uptake by cultured rat hypothalamic cells is regulated by intracellular cAMP.

Adenosine↗
PubMed1990

Induction by tumor necrosis factor-alpha of rapid release of immunoreactive and bioactive luteinizing hormone from rat pituitary cells in vitro.

Tumor necrosis factor-alpha (TNF-alpha) is secreted by activated monocytes and other immune cells. This paper reports studies on the effects of TNF-alpha on the releases of pituitary hormones such as luteinizing hormone (LH), follicle-stimulating hormone, prolactin (PRL) and adrenocorticotropic hormone (ACTH). The addition of recombinant human TNF-alpha (rTNF-alpha) to cultures of pituitary cells resulted in significantly increased releases of gonadotropins, PRL, and ACTH for up to 30 min, but not later. rTNF-alpha, like GnRH, also stimulated the release of bioactive LH. In addition, rTNF-alpha induced production of an interleukin-6 (IL-6)-like molecule by pituitary cells. As IL-6 induces the releases of multiple hormones from pituitary cells, our data suggest that rTNF-alpha may stimulate the releases of multiple pituitary hormones through IL-6 production as well as by its direct action on pituitary cells.

Adrenocorticotropic Hormone↗
PubMed1990

Electrocautery in polycystic ovary syndrome.

The serum levels of bioactive luteinizing hormone (LH), immunoreactive LH, follicle-stimulating hormone (FSH), and testosterone were determined in eleven anovulatory women with polycystic ovary syndrome (PCOS) before and after laparoscopic ovarian cautery. Before treatment, the mean +/- SEM levels of bioactive and immunoreactive LH and testosterone were 53.1 +/- 7.9 mIU/ml, 35.2 +/- 3.9 mIU/ml, and 1.14 +/- 0.13 ng/ml, respectively, which were significantly higher than those of five control women (19.2 +/- 1.6 mIU/ml, 21.4 +/- 1.2 mIU/ml, 0.28 +/- 0.03 ng/ml). After treatment, the mean levels of these hormones decreased significantly, ten women ovulated spontaneously and four conceived. The present results suggests that decreases in the levels of these hormones by laparoscopic ovarian cautery in women with PCOS may result in both restoration of the ovulatory cycle and the achievement of pregnancy.

Adult↗
PubMed1990

Trophoblast-derived interleukin-6 (IL-6) regulates human chorionic gonadotropin release through IL-6 receptor on human trophoblasts.

We examined the capacity of trophoblast-derived interleukin-6 (IL-6) to stimulate secretion of placental hormones, including hCG. IL-6 stimulated hCG secretion by trophoblasts to a level similar to that stimulated by a GnRH analog. The analog, however, released hCG by an IL-6-independent mechanism because PM-1, a monoclonal antibody specific for IL-6 receptors (R), failed to block GnRH-mediated responses, but completely blocked IL-6-mediated hCG secretion, suggesting the existence of two distinct regulatory pathways for hCG release. Immunohistochemical analysis with another IL-6-R-specific antibody, MT-18, showed that IL-6-R was located only on the trophoblast layer of the placenta. Our data revealed the existence of a local regulatory network by which trophoblast-derived IL-6 interacts with IL-6-R on the trophoblasts, resulting in hCG release. Thus, two different regulatory networks, an IL-6 and IL-6-R system and a GnRH and GnRH-R system, regulate hCG release by human trophoblasts independently.

Antibodies, Monoclonal↗
PubMed1990

5-Hydroxyeicosatetraenoic acid and phorbol ester stimulate prolactin release from rat anterior pituitary cells by different mechanisms.

The relationship between 5-hydroxyeicosatetraenoic acid (5-HETE) and calcium-activated, phospholipid-dependent protein kinase (protein kinase C) in prolactin (PRL) release was investigated in rat anterior pituitary cells. Arachidonic acid or 5-HETE, a 5-lipoxygenase metabolite of arachidonic acid, is known to cause a significant concentration-dependent increase in PRL release. Phorbol 12-myristate 13-acetate (PMA) and dioctanoyglycerol (diC8) have also been known to stimulate PRL release from pituitary cells, so we showed that these PRL releases were correlated with the activation of protein kinase C, that is, they induced dose-dependent translocation of protein kinase C from the cytosol to the membrane. Arachidonic acid, however, did not cause a significant change in the distribution of protein kinase C. We also showed that the PRL release induced by arachidonic acid and that induced by 5-HETE were additional to that by 100 nM PMA. Thus we suggested that the signals for the stimulation of PRL release sent by arachidonic acid and 5-HETE would be different from the signal sent through protein kinase C by PMA.

Animals↗
PubMed1990

Interleukin 6 possibly induced by interleukin 1 beta in the pituitary gland stimulates the release of gonadotropins and prolactin.

The abilities of recombinant human interleukin 1 (IL-1) and IL-6 to induce release of FSH, LH and PRL from rat pituitary cells in vitro were examined. IL-1 and IL-6 induced significant releases of FSH, LH and PRL within 3 h. The extents of release of these compounds induced by IL-1 and IL-6 were similar to those induced by GnRH and TRH. Rat anterior pituitary cells released IL-6 spontaneously, and its release was enhanced by IL-1 beta. This effect of IL-1 beta was inhibited significantly by a rabbit anti-IL-1 beta antiserum. These findings suggest that IL-1 induced the release of IL-6 from rat pituitary, and that the released IL-6 stimulated the secretions of FSH, LH and PRL.

Animals↗
PubMed1990

Interleukin 1 beta and tumour necrosis factor alpha stimulate the release of gonadotropin-releasing hormone and interleukin 6 by primary cultured rat hypothalamic cells.

The abilities of recombinant human interleukin 1 beta and tumour necrosis factor alpha to induce release of GnRH and interleukin 6 from primary culture of rat hypothalamic cells were examined. The effect of estradiol on the release of interleukin 6 by these cells was also tested. Both interleukin 1 beta and tumour necrosis factor alpha caused significant stimulation of GnRH secretion from the hypothalamic cells within 5 min. The hypothalamic cells secreted interleukin 6 spontaneously, and their secretion over 24 h was stimulated dose-dependently by interleukin 1 beta, tumour necrosis factor alpha and estradiol. These results suggest that interleukin 1 beta and tumour necrosis factor alpha stimulate the secretions of GnRH and interleukin 6 in the hypothalamus, and that these cytokines may be involved in the mechanism of GnRH secretion in the hypothalamus.

Animals↗
PubMed1990

Steroid hormones induce macrophage colony-stimulating factor (MCSF) and MCSF receptor mRNAs in the human endometrium.

We investigated the biological effects of sex-steroid hormones, secreted from the corpus luteum and placenta, on the induction of mRNAs encoding macrophage colony-stimulating factor (MCSF) and c-fms proto-oncogene (MCSF receptor) in human endometrium. RNA was extracted from the placenta and endometrium of both pregnant and non-pregnant women, and Northern blot analysis was performed on poly(A)+ RNA using MCSF or c-fms proto-oncogene cDNA as the probe. Results showed: (1) that MCSF mRNA was expressed in the placenta and endometrium of the pregnant uterus, (2) that c-fms proto-oncogene mRNA was also expressed in the placenta and endometrium of the pregnant uterus, and (3) that exogenous sex-steroid hormones could induce the expression of MCSF and c-fms proto-oncogene mRNAs in the endometrium of non-pregnant women. These results indicate that sex-steroid hormones secreted by the corpus luteum and/or placenta influence endometrial and placental growth and differentiation via a mechanism of action involving local production of MCSF and its receptor.

Corpus Luteum↗
PubMed1990

Physiologic thyroid activation in normal early pregnancy is induced by circulating hCG.

In normal early pregnancy, serum free thyroxine (T4) increases and serum TSH decreases, indicating that the thyroid gland is activated physiologically. To identify the factor responsible for this thyroid activation, we measured the serum thyroid-stimulating activity in comparison with the serum level of hCG in 39 normal women in early pregnancy. Serum thyroid-stimulating activity was measured by a sensitive cyclic adenosine 3',5'-monophosphate (cAMP) accumulation assay using a rat thyroid cell line (FRTL-5). Thyroid-stimulating activity was detected in 37 women (95%), and the activities of individuals correlated positively with their serum free T4 levels (r = 0.474; P less than .01) and negatively with their serum TSH levels (r = -0.376; P less than .02). Moreover, serum thyroid-stimulating activity correlated closely with the serum hCG level (r = 0.741; P less than .001), but was completely abolished by pre-treatment of the sera with hCG antibodies. These data indicate that in normal early pregnancy, the thyroid gland is physiologically activated by serum hCG, which has intrinsic thyroid-stimulating activity.

Animals↗
PubMed1990

[The clinical significance of serum sialyl Tn antigen levels in patients with gynecologic tumors].

In order to estimate the clinical significance of sialyl Tn (STN) antigen, the antigen was measured with an "STN" Otsuka Kit in sera from patients with various gynecologic tumors and healthy women. The antigen in ovarian fluid was also determined. Furthermore, the amount of serum STN antigen was serially checked in the patients with increased serum STN to evaluate the correlation between serum STN and the response to treatment. Results obtained were as follows. 1) Among the patients with uterine myoma, uterine malignancies and benign ovarian tumors, the incidence of increased serum STN antigen was low. 2) Among the patients with ovarian malignancies, serum STN antigen was significantly increased in the following order: Clinical stage I (18%) stage II (22%) stage III (68%). 3) The highest STN value was observed in the cyst fluid from ovarian malignancies. 4) The serum STN concentration was correlated with the effect of treatment. Interestingly, the increase in serum STN preceded the clinical detection of recurrence in one case. Thus STN appears to be a useful marker for monitoring ovarian malignancies.

Adult↗
PubMed1990

[Effect of low-dose aspirin therapy on utero-placental blood flow and malondialdehyde (MDA) as an indicator of its therapeutic effect].

Pregnancy-induced hypertension (PIH) and preeclampsia develop when an imbalance occurs between prostacyclin (PGI2) and thromboxane A2 (TXA2) production. PGI2 promotes vasodilation and decreases platelet adhesiveness, while TXA2 acts as a vasoconstrictor and enhances platelet aggregation and adhesion to vascular walls. The PGI2/TXA2 ratio appears to be important in pregnancy and the development of the functioning uteroplacental unit. Recently, antiplatelet treatment such as low-dose aspirin therapy has been effective in preventing the development of PIH and preeclampsia. TXA2 breaks down spontaneously into a stable substance, TXB2, which is inactive. Another stable, inactive metabolite, malondialdehyde (MDA), is formed via the same pathway. TXB2 and MDA are produced in approximately equimolar quantities. We studied the effects of a low-dose aspirin prescription. Production of MDA was remarkably suppressed during the low-dose aspirin therapy. Furthermore, pulsed doppler ultrasound assessment of blood flow was performed in the fetal descending aorta, umbilical artery and uterine artery of the low-dose aspirin therapy patients. Doppler abnormalities were improved during the therapy. It is concluded that low-dose aspirin improves the uteroplacental blood flow assessed by pulse doppler waveform and that determination of MDA is useful as an indicator of platelet thromboxane synthesis.

Adult↗