Search Results
You are looking at 1 - 7 of 7 items for
- Author: M Yoshida x
- Refine by access: All content x
Search for other papers by K. Mikami in
Google Scholar
PubMed
Search for other papers by M. Omura in
Google Scholar
PubMed
Search for other papers by Y. Tamura in
Google Scholar
PubMed
Search for other papers by S. Yoshida in
Google Scholar
PubMed
ABSTRACT
The site of action of 5-hydroperoxyeicosatetraenoic acid (5-HPETE) in ACTH-induced stimulation of steroidogenesis was examined in rat adrenocortical fasciculata cells. Prior addition of AA861, a specific inhibitor of 5-lipoxygenase, had no significant effect on cyclic AMP-dependent protein kinase activity and cholesterol esterase activities, when stimulated by ACTH in adrenocortical cells, compared with that stimulated by ACTH alone. Cholesterol accumulation in the mitochondria of cells treated with ACTH and cycloheximide was also not altered by pretreatment with AA861. We found, however, that pregnenolone formation, stimulated by ACTH, decreased in a dose-dependent manner when cells were pretreated with AA861. The inhibition of ACTH-stimulated pregnenolone formation by treatment with AA861 was restored only by prior addition of 5-HPETE. Furthermore, addition of AA861 also did not affect the conversion of pregnenolone into corticosterone.
In conclusion, 5-HPETE may act at the level of the mitochondria in ACTH-induced steroidogenesis in rat adrenal fasciculata cells.
Journal of Endocrinology (1990) 125, 89–96
Search for other papers by M. Nonomura in
Google Scholar
PubMed
Search for other papers by K. Hoshino in
Google Scholar
PubMed
Search for other papers by T. Harigaya in
Google Scholar
PubMed
Search for other papers by H. Hashimoto in
Google Scholar
PubMed
Search for other papers by O. Yoshida in
Google Scholar
PubMed
ABSTRACT
Hyperprolactinaemia induced by pituitary isografts in male host mice was confirmed by radioimmunoassay, but plasma testosterone levels determined by radioimmunoassay in these mice showed no changes. Immunoenzyme electron microscopic observations revealed large spherical-shaped immunoreactive prolactin granules in pituitary grafts in male hosts, regardless of the sex of the donor mice, indicating the disappearance of sexual dimorphism in prolactin-producing cells in hyperprolactinaemic mice. In hyperprolactinaemic host mice the male accessory sex glands, particularly the seminal vesicle and the ventral prostate, exhibited considerable proliferation and significant increase in weight. These phenomena do not seem to be mediated by the increased action of testosterone. Such biological effects in host mice were much greater when the donor was female rather than male, and were more noticeable in C57BL mice than in C3H mice.
J. Endocr. (1985) 107, 71–76
Search for other papers by K Katoh in
Google Scholar
PubMed
Search for other papers by M Yoshida in
Google Scholar
PubMed
Search for other papers by Y Kobayashi in
Google Scholar
PubMed
Search for other papers by M Onodera in
Google Scholar
PubMed
Search for other papers by K Kogusa in
Google Scholar
PubMed
Search for other papers by Y Obara in
Google Scholar
PubMed
In order to assess the biological significance of weaning and water deprivation on the control of plasma concentrations of adrenocorticotropic hormone (ACTH), cortisol, growth hormone (GH) and metabolites in response to stimulation with arginine-vasopressin (AVP) and corticotropin-releasing hormone (CRH), we carried out three experiments in which male goats before and after weaning were intravenously injected with AVP or CRH alone, or in combination with each other. In experiment 1, 17-week-old (post-weaning) goats were intravenously injected with AVP or CRH alone at the doses of 0.1, 0.3 and 1.0 nmol/kg body weight (BW). The AVP injection significantly and dose dependently increased plasma levels of ACTH, cortisol, GH and metabolites, whereas the injection with CRH did not cause significant increases in the levels of these parameters. In experiment 2, 4-week-old (pre-weaning) and 13-week-old (post-weaning) goats were injected with either AVP or CRH alone, followed by a combined injection of both secretagogues at a dose of 0.3 nmol/kg BW. Although the basal levels of the hormones and metabolites, with the exception of glucose, were greater in the 4-week-old goats, the hormone responses induced by stimulation with AVP were weaker than those induced in 13-week-old goats. Additionally, there were no responses in any hormone patterns to CRH stimulation in 4-week-old goats. In experiment 3, 13-week-old goats were injected with CRH alone followed by injection with AVP for two consecutive days of water deprivation. The animals were subjected to withdrawal of up to 20% of the total blood volume and water deprivation for up to 28 h. However, no significant differences in plasma ACTH, cortisol or GH levels were observed between days 1 and 2. Based on these results, we concluded that: (1) AVP is a more potent stimulant than CRH in terms of its ability to induce increases in plasma levels of ACTH, cortisol and GH; (2) the role of AVP as a secretagogue of hypothalamus–pituitary–adrenal hormones is strengthened, whereas the ineffective role of CRH remains unaltered, by weaning; (3) acute stress such as massive withdrawal of blood volume and subjection to water deprivation may not be sufficient burdens to alter stress-related hormone levels in young goats.
Search for other papers by H. Kaneko in
Google Scholar
PubMed
Search for other papers by M. Yoshida in
Google Scholar
PubMed
Search for other papers by Y. Hara in
Google Scholar
PubMed
Search for other papers by K. Taya in
Google Scholar
PubMed
Search for other papers by K. Araki in
Google Scholar
PubMed
Search for other papers by G. Watanabe in
Google Scholar
PubMed
Search for other papers by S. Sasamoto in
Google Scholar
PubMed
Search for other papers by Y. Hasegawa in
Google Scholar
PubMed
ABSTRACT
To investigate the physiological importance of inhibin in the regulation of FSH secretion in prepubertal bulls, animals (6-month-old) were passively immunized against inhibin. Five animals were given an i.v. bolus injection of 50 ml inhibin antiserum raised against bovine 32 kDa inhibin in a castrated male goat, and four bulls were given the same amount of castrated male goat serum (control serum) as controls. Treatment with the inhibin antiserum resulted in a marked increase (P < 0·01) in plasma concentrations of FSH within 12 h compared with control animals, and FSH levels in immunized animals remained high until 168 h after the injection. Concentrations of plasma LH and testosterone in the immunized animals were not different from those in the control animals. The present findings provide strong evidence that inhibin plays an important role in the inhibitory regulation of FSH secretion in prepubertal bulls.
Journal of Endocrinology (1993) 137, 15–19
Feed Functionality Research Laboratory, Meiji Feed Co., Kashima, Ibaraki 314-0103, Japan
Search for other papers by K Katoh in
Google Scholar
PubMed
Feed Functionality Research Laboratory, Meiji Feed Co., Kashima, Ibaraki 314-0103, Japan
Search for other papers by K Yoshioka in
Google Scholar
PubMed
Feed Functionality Research Laboratory, Meiji Feed Co., Kashima, Ibaraki 314-0103, Japan
Search for other papers by H Hayashi in
Google Scholar
PubMed
Feed Functionality Research Laboratory, Meiji Feed Co., Kashima, Ibaraki 314-0103, Japan
Search for other papers by T Mashiko in
Google Scholar
PubMed
Feed Functionality Research Laboratory, Meiji Feed Co., Kashima, Ibaraki 314-0103, Japan
Search for other papers by M Yoshida in
Google Scholar
PubMed
Feed Functionality Research Laboratory, Meiji Feed Co., Kashima, Ibaraki 314-0103, Japan
Search for other papers by Y Kobayashi in
Google Scholar
PubMed
Feed Functionality Research Laboratory, Meiji Feed Co., Kashima, Ibaraki 314-0103, Japan
Search for other papers by Y Obara in
Google Scholar
PubMed
Postprandial changes in plasma concentrations of GH, insulin, IGF-I, leptin and metabolites were compared between young Holstein bull calves fed with milk alone (control group) and with milk+5′-uridylic acid (UMP) (UMP group). UMP (2 g/day) was given with milk at 0830 h and 1530 h for 11 days from the 4th to the 14th day after birth. The perirenal fat weight was significantly lower in the UMP group than in the control group, but there was no significant difference in the weights of the liver, spleen and heart between the groups. Basal GH concentrations in the UMP group were slightly higher, but the postprandial increase in plasma insulin level and the area under the curve for insulin in the UMP group were significantly lower than those in the control group. There was no significant difference in IGF-I levels between the groups. In addition, the postprandial glucose concentrations were lower in the UMP group as reflected by the insulin level, and nonesterified fatty acid concentrations were not different. In the muscle (M. longissimus thoracis) sampled at 14 days of age, the triacylglycerol (TAG) content was significantly greater but glycogen content was significantly lower in the UMP group than in the control group. From these results, we have concluded that feeding 5′-UMP at 2 g/day for 11 days significantly alters TAG accumulation in the body and plasma concentrations of GH and insulin in young bull calves.
Search for other papers by A Mori-Abe in
Google Scholar
PubMed
Search for other papers by S Tsutsumi in
Google Scholar
PubMed
Search for other papers by K Takahashi in
Google Scholar
PubMed
Search for other papers by M Toya in
Google Scholar
PubMed
Search for other papers by M Yoshida in
Google Scholar
PubMed
Search for other papers by B Du in
Google Scholar
PubMed
Search for other papers by J Kawagoe in
Google Scholar
PubMed
Search for other papers by K Nakahara in
Google Scholar
PubMed
Search for other papers by T Takahashi in
Google Scholar
PubMed
Search for other papers by M Ohmichi in
Google Scholar
PubMed
Search for other papers by H Kurachi in
Google Scholar
PubMed
Proliferation of vascular smooth muscle cells (VSMC) plays a major role as an initiating event of atherosclerosis. Although estrogen directly inhibits the proliferation of VSMC, the mechanism has not been firmly established. In addition, the effect of raloxifene on VSMC remains unknown. 17Beta-estradiol (E(2)) and raloxifene significantly inhibited the growth of VSMC under growth-stimulated conditions. Since mitogen-activated protein (MAP) kinases have been implicated in VSMC proliferation, the role of MAP kinases in both the E(2)- and raloxifene-induced growth inhibition of VSMC was studied. Both E(2) and raloxifene caused rapid, transient phosphorylation and activation of p38 that was not affected by actinomycin D and was blocked by ICI 182,780. In contrast with p38 phosphorylation, extracellular signal-regulated protein kinase (ERK) phosphorylation was significantly inhibited and c-Jun N-terminal kinase (JNK) phosphorylation was not changed by E(2). Because VSMC expressed both estrogen receptor (ER) alpha and ERbeta, it is not known which of them mediates the E(2)-induced phosphorylation of p38. Although E(2) did not affect the p38 phosphorylation in A10 smooth muscle cells, which express ERbeta but not ERalpha, transfection of ERalpha expression vector into A10 cells rendered them susceptible to induction of p38 phosphorylation by E(2). We then examined whether E(2) and raloxifene induce apoptosis through a p38 cascade. Both E(2) and raloxifene induced apoptosis under growth-stimulated conditions. The p38 inhibitor SB 203580 completely blocked the E(2)-induced apoptosis. Our findings suggest that both E(2)- and raloxifene-induced inhibition of VSMC growth is due to induction of apoptosis through a p38 cascade whose activation is mediated by ERalpha via a nongenomic mechanism.
Search for other papers by K Takahashi in
Google Scholar
PubMed
Search for other papers by M Ohmichi in
Google Scholar
PubMed
Search for other papers by M Yoshida in
Google Scholar
PubMed
Search for other papers by K Hisamoto in
Google Scholar
PubMed
Search for other papers by S Mabuchi in
Google Scholar
PubMed
Search for other papers by E Arimoto-Ishida in
Google Scholar
PubMed
Search for other papers by A Mori in
Google Scholar
PubMed
Search for other papers by S Tsutsumi in
Google Scholar
PubMed
Search for other papers by K Tasaka in
Google Scholar
PubMed
Search for other papers by Y Murata in
Google Scholar
PubMed
Search for other papers by H Kurachi in
Google Scholar
PubMed
The proliferation of vascular smooth muscle cells (VSMC) is a crucial pathophysiological process in the development of atherosclerosis. Although estrogen is known to inhibit the proliferation of VSMC, the mechanism responsible for this effect remains to be elucidated. In addition, the effect of raloxifene on VSMC remains unknown. We have shown here that 17beta-estradiol (E(2)) and raloxifene significantly inhibited the platelet-derived growth factor (PDGF)-stimulated proliferation of cultured human VSMC. Flow cytometry demonstrated that PDGF-stimulated S-phase progression of the cell cycle in VSMC was also suppressed by E(2) or raloxifene. We found that PDGF-induced phosphorylation of retinoblastoma protein (pRb), whose hyperphosphorylation is a hallmark of the G1-S transition in the cell cycle, was significantly inhibited by E(2) and raloxifene. These effects were associated with a decrease in cyclin D1 expression, without a change in cyclin-dependent kinase 4 or cyclin-dependent kinase inhibitor, p27(kip1) expression. ICI 182,780 abolished the inhibitory effects of E(2) and raloxifene on PDGF-induced pRb phosphorylation. Next, we examined which estrogen receptor (ER) is necessary for these effects of E(2) and raloxifene. Since VSMC express both ERalpha and ERbeta, A10, a rat aortic smooth muscle cell line that expresses ERbeta but not ERalpha, was used. The dose-dependent stimulation of A10 cell proliferation by PDGF was not inhibited by E(2) or raloxifene in contrast to the results obtained in VSMC. Moreover, E(2) and raloxifene significantly inhibited the PDGF-induced cyclin D1 promoter activity in A10 cells transfected with cDNA for ERalpha but not in the parental cells. These results suggested that E(2) and raloxifene exert an antiproliferative effect in VSMC treated with PDGF, at least in part through inhibition of pRb phosphorylation, and that the inhibitory effects of E(2) and raloxifene may be mainly mediated by ERalpha.
