The Experts below are selected from a list of 102 Experts worldwide ranked by ideXlab platform
Haruhiko Kanasaki - One of the best experts on this subject based on the ideXlab platform.
-
Role of thyrotropin-releasing hormone in Prolactin-producing cell models
Neuropeptides, 2015Co-Authors: Haruhiko Kanasaki, Tselmeg Mijiddorj, Aki Oride, Satoru KyoAbstract:Thyrotropin-releasing hormone (TRH) is a hypothalamic hypophysiotropic neuropeptide that was named for its ability to stimulate the release of thyroid-stimulating hormone in mammals. It later became apparent that it exerts a number of species-dependent hypophysiotropic activities that regulate other pituitary hormones. TRH also regulates the Synthesis and release of Prolactin, although whether it is a physiological regulator of Prolactin that remains unclear. Occupation of the Gq protein-coupled TRH receptor in the Prolactin-producing lactotroph increases the turnover of inositol, which in turn activates the protein kinase C pathway and the release of Ca(2+) from storage sites. TRH-induced signaling events also include the activation of extracellular signal-regulated kinase (ERK) and induction of MAP kinase phosphatase, an inactivator of activated ERK. TRH stimulates Prolactin Synthesis through the activation of ERK, whereas Prolactin release occurs via elevation of intracellular Ca(2+). We have been investigating the role of TRH in a pituitary Prolactin-producing cell model. Rat pituitary somatolactotroph GH3 cells, which produce and release both Prolactin and growth hormone (GH), are widely used as a model for the study of Prolactin- and GH-secreting cells. In this review, we describe the general action of TRH as a hypophysiotropic factor in vertebrates and focus on the role of TRH in Prolactin Synthesis using GH3 cells.
-
Stimulatory effect of pituitary adenylate-cyclase activating polypeptide (PACAP) and its PACAP type I receptor (PAC1R) on Prolactin Synthesis in rat pituitary somatolactotroph GH3 cells.
Molecular and cellular endocrinology, 2011Co-Authors: Tselmeg Mijiddorj, Haruhiko Kanasaki, Indri N Purwana, Aki Oride, Kohji MiyazakiAbstract:In this present study, we investigated the role of pituitary adenylate cyclase-activating polypeptide (PACAP) and its receptor, PACAP type I receptor (PAC1R) on Prolactin Synthesis in pituitary somatolactotroph GH3 cells. PACAP increased Prolactin promoter activity up to 1.3 ± 0.1-fold. This increase, while significant, was less than the increase resulting from thyrotropin-releasing hormone (TRH) stimulation. By transfection of a PAC1R expression vector to the cells, the response to PACAP on Prolactin promoter activity was dramatically potentiated to a degree proportional to the amount of PAC1R transfected. In the PAC1R expressing GH3 cells, TRH and PACAP alone increased Prolactin promoter up to 3.3 ± 0.3-fold and 4.9 ± 0.2-fold, respectively, and combined treatment with TRH and PACAP further increased Prolactin promoters up to 6.8 ± 0.6-fold. PACAP binds both Gs- and Gq-coupled receptors and stimulates adenylate cyclase/cAMP and protein kinase C/extracellular signal-regulated kinase (ERK) signaling pathways. PACAP increased ERK phosphorylation in PAC1R expressing cells to the same degree as TRH. Combined treatment with TRH and PACAP had a synergistic effect on ERK activation. GH3 cells produce both Prolactin and growth hormone. Stimulation of GH3 cells with TRH significantly increased the mRNA level of Prolactin and attenuated growth hormone mRNA expression. PACAP increased both Prolactin and growth hormone mRNA levels, particularly in PAC1R expressing cells. In addition, increasing amount of PAC1R in GH3 cells potentiated the action of TRH on Prolactin promoter activity, as well as on ERK phosphorylation. PAC1R was induced by PACAP itself, but not by TRH. Our current study demonstrates that PACAP and its PAC1R, functions as a stimulator of Prolactin alone or with TRH in Prolactin producing cells.
Satoru Kyo - One of the best experts on this subject based on the ideXlab platform.
-
Role of thyrotropin-releasing hormone in Prolactin-producing cell models
Neuropeptides, 2015Co-Authors: Haruhiko Kanasaki, Tselmeg Mijiddorj, Aki Oride, Satoru KyoAbstract:Thyrotropin-releasing hormone (TRH) is a hypothalamic hypophysiotropic neuropeptide that was named for its ability to stimulate the release of thyroid-stimulating hormone in mammals. It later became apparent that it exerts a number of species-dependent hypophysiotropic activities that regulate other pituitary hormones. TRH also regulates the Synthesis and release of Prolactin, although whether it is a physiological regulator of Prolactin that remains unclear. Occupation of the Gq protein-coupled TRH receptor in the Prolactin-producing lactotroph increases the turnover of inositol, which in turn activates the protein kinase C pathway and the release of Ca(2+) from storage sites. TRH-induced signaling events also include the activation of extracellular signal-regulated kinase (ERK) and induction of MAP kinase phosphatase, an inactivator of activated ERK. TRH stimulates Prolactin Synthesis through the activation of ERK, whereas Prolactin release occurs via elevation of intracellular Ca(2+). We have been investigating the role of TRH in a pituitary Prolactin-producing cell model. Rat pituitary somatolactotroph GH3 cells, which produce and release both Prolactin and growth hormone (GH), are widely used as a model for the study of Prolactin- and GH-secreting cells. In this review, we describe the general action of TRH as a hypophysiotropic factor in vertebrates and focus on the role of TRH in Prolactin Synthesis using GH3 cells.
Tselmeg Mijiddorj - One of the best experts on this subject based on the ideXlab platform.
-
Role of thyrotropin-releasing hormone in Prolactin-producing cell models
Neuropeptides, 2015Co-Authors: Haruhiko Kanasaki, Tselmeg Mijiddorj, Aki Oride, Satoru KyoAbstract:Thyrotropin-releasing hormone (TRH) is a hypothalamic hypophysiotropic neuropeptide that was named for its ability to stimulate the release of thyroid-stimulating hormone in mammals. It later became apparent that it exerts a number of species-dependent hypophysiotropic activities that regulate other pituitary hormones. TRH also regulates the Synthesis and release of Prolactin, although whether it is a physiological regulator of Prolactin that remains unclear. Occupation of the Gq protein-coupled TRH receptor in the Prolactin-producing lactotroph increases the turnover of inositol, which in turn activates the protein kinase C pathway and the release of Ca(2+) from storage sites. TRH-induced signaling events also include the activation of extracellular signal-regulated kinase (ERK) and induction of MAP kinase phosphatase, an inactivator of activated ERK. TRH stimulates Prolactin Synthesis through the activation of ERK, whereas Prolactin release occurs via elevation of intracellular Ca(2+). We have been investigating the role of TRH in a pituitary Prolactin-producing cell model. Rat pituitary somatolactotroph GH3 cells, which produce and release both Prolactin and growth hormone (GH), are widely used as a model for the study of Prolactin- and GH-secreting cells. In this review, we describe the general action of TRH as a hypophysiotropic factor in vertebrates and focus on the role of TRH in Prolactin Synthesis using GH3 cells.
-
Stimulatory effect of pituitary adenylate-cyclase activating polypeptide (PACAP) and its PACAP type I receptor (PAC1R) on Prolactin Synthesis in rat pituitary somatolactotroph GH3 cells.
Molecular and cellular endocrinology, 2011Co-Authors: Tselmeg Mijiddorj, Haruhiko Kanasaki, Indri N Purwana, Aki Oride, Kohji MiyazakiAbstract:In this present study, we investigated the role of pituitary adenylate cyclase-activating polypeptide (PACAP) and its receptor, PACAP type I receptor (PAC1R) on Prolactin Synthesis in pituitary somatolactotroph GH3 cells. PACAP increased Prolactin promoter activity up to 1.3 ± 0.1-fold. This increase, while significant, was less than the increase resulting from thyrotropin-releasing hormone (TRH) stimulation. By transfection of a PAC1R expression vector to the cells, the response to PACAP on Prolactin promoter activity was dramatically potentiated to a degree proportional to the amount of PAC1R transfected. In the PAC1R expressing GH3 cells, TRH and PACAP alone increased Prolactin promoter up to 3.3 ± 0.3-fold and 4.9 ± 0.2-fold, respectively, and combined treatment with TRH and PACAP further increased Prolactin promoters up to 6.8 ± 0.6-fold. PACAP binds both Gs- and Gq-coupled receptors and stimulates adenylate cyclase/cAMP and protein kinase C/extracellular signal-regulated kinase (ERK) signaling pathways. PACAP increased ERK phosphorylation in PAC1R expressing cells to the same degree as TRH. Combined treatment with TRH and PACAP had a synergistic effect on ERK activation. GH3 cells produce both Prolactin and growth hormone. Stimulation of GH3 cells with TRH significantly increased the mRNA level of Prolactin and attenuated growth hormone mRNA expression. PACAP increased both Prolactin and growth hormone mRNA levels, particularly in PAC1R expressing cells. In addition, increasing amount of PAC1R in GH3 cells potentiated the action of TRH on Prolactin promoter activity, as well as on ERK phosphorylation. PAC1R was induced by PACAP itself, but not by TRH. Our current study demonstrates that PACAP and its PAC1R, functions as a stimulator of Prolactin alone or with TRH in Prolactin producing cells.
Aki Oride - One of the best experts on this subject based on the ideXlab platform.
-
Role of thyrotropin-releasing hormone in Prolactin-producing cell models
Neuropeptides, 2015Co-Authors: Haruhiko Kanasaki, Tselmeg Mijiddorj, Aki Oride, Satoru KyoAbstract:Thyrotropin-releasing hormone (TRH) is a hypothalamic hypophysiotropic neuropeptide that was named for its ability to stimulate the release of thyroid-stimulating hormone in mammals. It later became apparent that it exerts a number of species-dependent hypophysiotropic activities that regulate other pituitary hormones. TRH also regulates the Synthesis and release of Prolactin, although whether it is a physiological regulator of Prolactin that remains unclear. Occupation of the Gq protein-coupled TRH receptor in the Prolactin-producing lactotroph increases the turnover of inositol, which in turn activates the protein kinase C pathway and the release of Ca(2+) from storage sites. TRH-induced signaling events also include the activation of extracellular signal-regulated kinase (ERK) and induction of MAP kinase phosphatase, an inactivator of activated ERK. TRH stimulates Prolactin Synthesis through the activation of ERK, whereas Prolactin release occurs via elevation of intracellular Ca(2+). We have been investigating the role of TRH in a pituitary Prolactin-producing cell model. Rat pituitary somatolactotroph GH3 cells, which produce and release both Prolactin and growth hormone (GH), are widely used as a model for the study of Prolactin- and GH-secreting cells. In this review, we describe the general action of TRH as a hypophysiotropic factor in vertebrates and focus on the role of TRH in Prolactin Synthesis using GH3 cells.
-
Stimulatory effect of pituitary adenylate-cyclase activating polypeptide (PACAP) and its PACAP type I receptor (PAC1R) on Prolactin Synthesis in rat pituitary somatolactotroph GH3 cells.
Molecular and cellular endocrinology, 2011Co-Authors: Tselmeg Mijiddorj, Haruhiko Kanasaki, Indri N Purwana, Aki Oride, Kohji MiyazakiAbstract:In this present study, we investigated the role of pituitary adenylate cyclase-activating polypeptide (PACAP) and its receptor, PACAP type I receptor (PAC1R) on Prolactin Synthesis in pituitary somatolactotroph GH3 cells. PACAP increased Prolactin promoter activity up to 1.3 ± 0.1-fold. This increase, while significant, was less than the increase resulting from thyrotropin-releasing hormone (TRH) stimulation. By transfection of a PAC1R expression vector to the cells, the response to PACAP on Prolactin promoter activity was dramatically potentiated to a degree proportional to the amount of PAC1R transfected. In the PAC1R expressing GH3 cells, TRH and PACAP alone increased Prolactin promoter up to 3.3 ± 0.3-fold and 4.9 ± 0.2-fold, respectively, and combined treatment with TRH and PACAP further increased Prolactin promoters up to 6.8 ± 0.6-fold. PACAP binds both Gs- and Gq-coupled receptors and stimulates adenylate cyclase/cAMP and protein kinase C/extracellular signal-regulated kinase (ERK) signaling pathways. PACAP increased ERK phosphorylation in PAC1R expressing cells to the same degree as TRH. Combined treatment with TRH and PACAP had a synergistic effect on ERK activation. GH3 cells produce both Prolactin and growth hormone. Stimulation of GH3 cells with TRH significantly increased the mRNA level of Prolactin and attenuated growth hormone mRNA expression. PACAP increased both Prolactin and growth hormone mRNA levels, particularly in PAC1R expressing cells. In addition, increasing amount of PAC1R in GH3 cells potentiated the action of TRH on Prolactin promoter activity, as well as on ERK phosphorylation. PAC1R was induced by PACAP itself, but not by TRH. Our current study demonstrates that PACAP and its PAC1R, functions as a stimulator of Prolactin alone or with TRH in Prolactin producing cells.
Isabella Caroline Mcmillen - One of the best experts on this subject based on the ideXlab platform.
-
The relative roles of the hypothalamus and cortisol in the control of Prolactin gene expression in the anterior pituitary of the sheep fetus.
Journal of neuroendocrinology, 1996Co-Authors: I. D. Phillips, S. L. Fielke, I. R. Young, Isabella Caroline McmillenAbstract:The neuroendocrine control of Prolactin Synthesis and secretion before birth is not well understood. We have measured the changes in the level of Prolactin mRNA in the anterior pituitary of the fetal sheep throughout the last 15 days of pregnancy (term = 147 +/- 3 days gestation). We have also investigated the effects of surgical disconnection of the fetal hypothalamus and pituitary (HPD) with or without long term cortisol infusion on pituitary Prolactin mRNA levels and plasma Prolactin concentrations in the late gestation sheep fetus. Prolactin mRNA levels were measured in anterior pituitaries collected from a series of fetal sheep (130-134 days, n = 6; 135-140 days, n = 6; 141-145 days, n = 6) in late gestation. HPD was carried out in ten fetal sheep at 105-115 days gestation and five intact fetal sheep were used as controls. In the HPD group, either saline (HPD + saline group, n = 5) or cortisol was infused (3.5 mg/24 h) for 5 days from 134-136 days gestation (HPD + cortisol group, n = 5). There was an increase in the ratio of Prolactin mRNA: 18S rRNA in the fetal pituitary between 130-134 days (0.46 +/- 0.08, n = 6) and 135-140 days (1.27 +/- 0.17 n = 6) which was maintained after 141 days gestation, (1.27 +/- 0.11, n = 6). The mean Prolactin mRNA: 18 S rRNA ratio was significantly higher (P < 0.05) in intact fetal sheep (1.41 +/- 0.16, n = 4) than in the HPD fetal sheep after either saline (0.54 +/- 0.14, n = 4) or cortisol (0.74 +/- 0.24, n = 5) administration. The mean plasma concentration of Prolactin was also higher in the intact group (28.3 +/- 3.9 ng/ml) when compared with the HPD + saline group (8.0 +/- 3.3 ng/ml) or the HPD + cortisol group (5.6 +/- 1.9 ng/ml). We have demonstrated that there is a strong hypothalamic drive to Prolactin Synthesis and secretion in the fetus and that cortisol does not act directly at the fetal pituitary to stimulate Prolactin Synthesis and secretion in late gestation.
