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N. Sugino, H. Tamura, Y. Nakamura, K. Ueda, and H. Kato

ABSTRACT

The present study investigated possible sites through which ACTH or corticosterone inhibit progesterone secretion in pregnant rats, and the role of placental factors in blocking the inhibitory effect. The number of conceptuses was adjusted to one (1C group) or more than ten (FC group) on day 7 of pregnancy by aspirating the desired number. Serum concentrations of progesterone, testosterone and oestradiol were significantly (P<0·01) lower on day 15 in the 1C group than in the FC group. Corpora lutea (CL) obtained on day 15 were incubated for 6 h with corticosterone or ACTH. Corticosterone (1 μmol/l) significantly (P<0·05) inhibited progesterone secretion in the IC group but not in the FC group. The inhibitory effect of corticosterone in the IC group was completely blocked by co-addition of 1 μmol testosterone/l or 1 μmol oestradiol/l but not by 1 μmol dihydrotestosterone/l. ACTH (1 μg/l–1 mg/l) had no direct effect on progesterone secretion in either the IC or the FC groups, although ACTH apparently decreases progesterone secretion in vivo. Placentae obtained from rats of the FC group on day 15 were incubated for 24 h with or without ACTH (1 mg/l). The supernatant after placental incubation without ACTH significantly (P<0·01) increased progesterone secretion by the CL in both the IC and FC groups, and also eliminated the inhibitory effect of corticosterone in the IC group. The supernatant after placental incubation with ACTH also increased progesterone secretion in the FC group as effectively as the supernatant from the control incubation, but it had no effect in the IC group. It is concluded that corticosterone directly inhibits progesterone secretion by the CL, whereas the inhibitory effect of ACTH is mediated through the placenta. The results indicate that these inhibitory effects of corticosterone or ACTH are eliminated if the CL has been exposed to enough placental hormones before day 15 of pregnancy.

Journal of Endocrinology (1991) 129, 405–410

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H Shimizu, K Ohtani, Y Kato, and M Mori

Interleukin (IL)-6, one of the cytokines released from inflammatory cells, stimulates insulin secretion in a physiological concentration (1-100 pg/ml), but the exact mechanism is still unknown. The present studies were undertaken to investigate the mechanism of IL-6-induced stimulation of insulin secretion in HIT-T 15 cells. The effects of the addition of nifedipine on the IL-6 (100 pg/ml)-induced stimulation of insulin secretion were investigated. We also examined the possibility that IL-6 (1-100 pg/ml) may stimulate insulin messenger ribonucleic acid (mRNA) expression, using the reverse transcription-polymerase chain reaction method. The addition of 100 and 1000 nM nifedipine significantly attenuated the stimulatory effects of 100 pg/ml IL-6 on insulin secretion. The addition of 1-100 pg/ml IL-6 dose-dependently increased preproinsulin mRNA expression relative to beta-actin mRNA. IL-6 increased insulin gene promoter activity of fragments A (-2188 to +337 bp) and B (-1782 to +270 bp) but not fragments C (-1275 to +270 bp), D (-1138 to +270 bp), E (-880 to +236 bp) or F (-356 to +252 bp). The addition of 10 nM nifedipine completely abolished the stimulatory effect of 10-100 pg/ml IL-6 on relative preproinsulin mRNA expression. These data raised the possibility that IL-6 increased preproinsulin mRNA expression via the stimulation of Ca(2+) influx which enhances insulin gene expression.

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M Imae, Y Inoue, Z Fu, H Kato, and T Noguchi

Hepatocyte nuclear factor-3 (HNF-3) belongs to a large family of forkhead transcription factors and is made up of three members (HNF-3alpha, -3beta and -3gamma). It has been shown that HNF-3 regulates a number of metabolically important genes. However, the mechanisms underlying this regulation of HNF-3 activity by hormones and nutrition have not yet been well elucidated. In attempting to explore the regulation of gene expression of HNF-3 members by physiological status, we analyzed the effects of insulin, dexamethasone and protein malnutrition on the hepatic mRNA level of each member. Male Wistar rats were fed on a 12% casein diet, 12% gluten diet (deficient in lysine and threonine) or a protein-free diet for 1 week. The protein-free diet and gluten diet caused a 3. 7-fold increase in HNF-3g mRNA in the liver and did not affect the mRNA level of either HNF-3alpha or HNF-3beta. Daily administration of dexamethasone caused the mRNA levels of HNF-3alpha and HNF-3beta to increase (2.3- and 1.4-fold, respectively), but had no effect on the HNF-3gamma mRNA level. In diabetic rats that had been injected with streptozotocin, an elevation of the hepatic mRNA levels of HNF-3beta and HNF-3gamma was observed (1.6-and 1.9-fold, respectively). Insulin replacement in the diabetic rats decreased both mRNA levels in a dose-dependent manner. HNF-3alpha mRNA was not affected by insulin status. These results show that the genes of the three members of the HNF-3 family respond differently to hormonal and nutritional factors suggesting that the activities of HNF-3 members are regulated, at least in part, by the levels of their gene expression.

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M. Kato, M. Hagiwara, Y. Nimura, S. Shionoya, and H. Hidaka

ABSTRACT

Calmodulin has been identified in parathyroid cells and is thought to play an important role in the production or secretion of parathyroid hormone. However, a detailed investigation of calmodulinbinding proteins in parathyroid glands has not been conducted. In this study, we attempted to determine the presence of calmodulin-binding protein in human parathyroid adenoma by affinity chromatography. The eluted protein from a calmodulin-coupled Sepharose 4B column with EGTA was analysed by sodium dodecyl sulphate-polyacrylamide gel electrophoresis which revealed a major protein band of M r 50 000. A Ca2+/calmodulin-dependent protein kinase activity was detected at the protein peak using dephosphorylated casein as a substrate. The 50 kDa band was identified as calcium/calmodulin-dependent protein kinase II (CaM-kinase II) by immunoblotting. The substrate specificity, pH dependency and affinity for calmodulin of this enzyme were identical to those of CaM-kinase II from rat brain. Also, the kinase activity was sensitive to KN-62, a specific inhibitor of CaM-kinase II. In total, 0·48 mg of this kinase was purified from 3 g human parathyroid adenoma.

Journal of Endocrinology (1991) 131, 155–162

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ZW Fu, T Kubo, K Sugahara, T Noguchi, and H Kato

We investigated the effects of vitamin A (VA) nutritional status on the levels of expression of retinoic acid (RA) receptor-beta (RARbeta) gene in the various tissues of Japanese quail. VA deficiency caused a significant decrease in the mRNA levels of brain, liver, heart, lung and kidney RARbeta2/beta4, whereas no change was observed in the level of testis RARbeta2 transcript. In contrast, reduction in the RARbeta1 transcript caused by VA depletion was observed only in the lung, remaining unchanged in the other tissues. The administration of RA to the VA-deficient quail rapidly induced the expression of RARbeta2/beta4 mRNAs in all the tissues examined, but RA increased the expression of RARbeta1 transcript in the liver, heart, lung and kidney at a lower magnitude. RA could not change the expression of the brain RARbeta1 transcript, while it induced the expression of the testis RARbeta1 mRNA in a temporal way. These results clearly indicate that VA nutritional status differently regulates the expression of RARbeta1 and RARbeta2/beta4 transcripts in a tissue-specific manner.

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F. Miyauchi, H. Kato, H. Yamashita, K. Ueda, H. Tamura, T. Mano, and T. Torigoe

ABSTRACT

The effects of a conceptus-derived substance on the activity of 3β-hydroxysteroid dehydrogenase (3β-HSD) and 20α-HSD in the ovary were studied in the rat. On day 7 of pregnancy (day 1 = insemination), rats were laparotomized and the desired number of conceptuses was aspirated from the uterus; thus, rats carrying one, two, three, four, five to seven or eight to ten conceptuses were prepared. They were autopsied on day 15 and 3β-HSD and 20α-HSD activity in the corpus luteum (CL) or non-luteal ovarian tissue (NLO) was determined. Conceptus number was directly related to 3β-HSD and inversely related to 20α-HSD activity in the CL. The serum progesterone level and CL weight were also directly related to conceptus number. Neither 3β-HSD nor 20α-HSD activity in the NLO was affected by conceptus number. These results indicated that 3β-HSD and 20α-HSD in the CL are probably regulated by placental hormone secreted in proportion to the number of conceptuses; in the NLO these enzymes may be controlled by a different mechanism.

J. Endocr. (1984) 101, 285–288

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M. Ohashi, N. Fujio, K. Kato, H. Nawata, H. Ibayashi, and H. Matsuo

ABSTRACT

To determine the effects of atrial natriuretic polypeptide (ANP) on plasma levels of ACTH, cortisol, aldosterone and dehydroepiandrosterone (DHEA), synthetic human α-ANP (hα-ANP) was infused i.v. into eight normotensive, disease-free volunteers, at a dose and duration previously found to be sufficient to produce apparent cardiovascular and renal effects.

The mean basal concentration of plasma ACTH determined by radioimmunoassay was 18·2 ± 3·1 ng/l. Plasma ACTH concentrations tended to be decreased during the infusion in all subjects. However, the change in plasma ACTH concentrations during infusion of hα-ANP was essentially the same as that during the infusion of saline. The mean plasma cortisol concentration was significantly suppressed from 25 to 40 min after the end of synthetic hα-ANP infusion. At 90 min after infusion, the mean plasma level of cortisol reverted to the pretreatment level. There was a non-significant increase in plasma renin activity following the infusion. The mean plasma aldosterone concentration was reduced by 15% (P < 0·05) during the infusion and returned to preinfusion levels 10 min after termination of the infusion, after which the mean plasma concentration declined to the level seen during infusion. Administration of hα-ANP had no significant influence on plasma DHEA concentrations, but there was a tendency to decrease during the infusion.

Our data suggest that synthetic hα-ANP inhibits adrenocortical steroidogenesis in man.

J. Endocr. (1986) 110, 287–292

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H Tokuda, O Kozawa, M Niwa, H Matsuno, K Kato, and T Uematsu

We investigated the effect of prostaglandin E2 (PGE2) on the induction of heat shock protein 27 (HSP27) and HSP70, and the mechanism behind the induction in osteoblast-like MC3T3-E1 cells. PGE2 time-dependently increased the level of HSP27 without affecting the level of HSP70. PGE2 stimulated the accumulation of HSP27 dose-dependently in the range between 10 nM and 10 microM. PGE2 stimulated the increase in the level of the mRNA for HSP27. Staurosporine and calphostin C, inhibitors of protein kinase C (PKC), suppressed the PGE2-induced HSP27 accumulation. The effect of PGE2 on HSP27 accumulation was reduced in the PKC down-regulated cells. BAPTA/AM, a chelator of intracellular Ca2+, or TMB-8, an inhibitor of intracellular Ca2+ mobilization, reduced the accumulation of HSP27 induced by PGE2. Dibutyryl cAMP had little effect on the basal level of HSP27. PGE2 induced the phosphorylation of both p44/p42 mitogen-activated protein (MAP) kinase and p38 MAP kinase. PD98059 and U-0126, inhibitors of the upstream kinase of p44/p42 MAP kinase, reduced the accumulation of HSP27 induced by PGE2. SB203580, a specific inhibitor of p38 MAP kinase, suppressed the HSP27 accumulation induced by PGE2. U-73122, an inhibitor of phospholipase C, and calphostin C reduced the PGE2-induced phosphorylation of both p44/p42 MAP kinase and p38 MAP kinase. These results indicate that PGE2 stimulates the induction of HSP27 through PKC-dependent activations of both p44/p42 MAP kinase and p38 MAP kinase in osteoblasts.

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Y Nakamura, H Tamura, M Ono, K Shimamura, N Sugino, F Numa, K Ueda, and H Kato

Abstract

The purpose of this study was to examine the possible mechanism through which RU486 induces luteolysis during the late-luteal phase in pseudopregnant (PSP) rats. PSP rats received a subcutaneous injection of RU486 in sesame oil (5 mg/kg body weight) or sesame oil alone once a day between day 9 and day 11 of pseudopregnancy. Serial blood samples were collected on days 5, 9, 10, 11 and 12 and assayed for progesterone content. To examine the possible action of RU486 through a uterine and/or a pituitary (prolactin-dependent) mechanism, PSP rats and chronic hysterectomized PSP rats which had been hysterectomized before PSP induction received a subcutaneous injection of RU486 in sesame oil (5 mg/kg body weight), sesame oil alone, prolactin in 50% polyvinylpyrrolidone (15 IU/day), or RU486 and prolactin once a day between day 9 and day 11 of pseudopregnancy. Serial blood samples were collected on days 5, 9, 10 and 11 and assayed for progesterone content. Blood samples were also collected at 0400 h on day 12 and used for prolactin and progesterone determinations. To examine the direct effect of RU486 on corpus luteum and/or pituitary, hysterectomized rats underwent hypophysectomy and pituitary autotransplantation on dioestrus 1 and received a subcutaneous injection of RU486 in sesame oil or sesame oil alone for 3 days between day 21 and day 23 after surgery. Serial blood samples were collected on days 10, 21, 22, 23 and 24 and assayed for progesterone and prolactin contents.

In ordinary PSP rats, serum progesterone levels were significantly (P<0·01) lower in the RU486-treated group than in the control group (9 ± 1 vs 53 ± 7 ng/ml; mean ± s.e.m.) on day 11. Serum prolactin levels at 0400 h on day 12 of pseudopregnancy were significantly (P<0·05) lower in the RU486-treated group than in the control group (16 ±4 vs 154 ±44 ng/ml; mean ± s.e.m.). The concomitant prolactin treatment reversed the luteolytic effects of RU486 on day 11 of pseudopregnancy. In hysterectomized PSP rats, RU486 also suppressed serum prolactin levels, and the concomitant prolactin treatment again reversed the luteolytic effects of RU486. In hysterectomized rats which were hypophysectomized and pituitary autotransplanted, RU486 treatment did not induce any significant changes in serum progesterone and prolactin levels.

These results indicated that RU486 induced luteolysis during the late-luteal phase in PSP rats by suppressing prolactin secretion via a hypothalamic mechanism.

Journal of Endocrinology (1996) 150, 93–98

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Y Ninomiya, Y Arao, T Kometani, S Hiwatashi, T Yamasaki, T Erikawa, H Yamaguchi, T Hasegawa, S Masushige, and S Kato

Abstract

We examined vitamin A-deficient chicks to determine whether vitamin A affects the estrogen-induced development of the chick oviduct. When oviduct development was stimulated for 5 days with the synthetic estrogen, diethylstilbestrol, the wet weight of the oviduct in vitamin A-deficient chicks was only half that in control chicks. The DNA content in this tissue showed that the decreased oviduct weight in the vitamin A-deficient chicks was caused by the decreased proliferation of oviduct cells. However, the estrogen-induced expression of the ovalbumin gene was not affected by the vitamin A deficiency, suggesting that estrogen-induced cytodifferentiation is not affected by vitamin A. To clarify the vitamin A action on estrogen-induced development in the oviduct, transcripts of nuclear estrogen receptor (ER) and all-trans-retinoic acid (RARα, β and γ) receptors, which exert the effects of estrogen and vitamin A, were measured. The ER, RARα and RARβ genes, but not that of RARγ, were expressed during oviduct development, indicating that estrogen and vitamin A may control the expression of target genes through their cognate receptors. Thus, we have shown that vitamin A is involved in estrogen-induced cell proliferation but not in cytodifferentiation of the chicken oviduct.

Journal of Endocrinology (1996) 148, 257–265