scholarly journals Administration of Adrenocorticotropic Hormone during Chicken Embryonic Development Prematurely Induces Pituitary Growth Hormone Cells

Endocrinology ◽  
2007 ◽  
Vol 148 (8) ◽  
pp. 3914-3921 ◽  
Author(s):  
S. A. Jenkins ◽  
M. Muchow ◽  
M. P. Richards ◽  
J. P. McMurtry ◽  
T. E. Porter
Keyword(s):  
Cell Differentiation ◽  
Adrenal Gland ◽  
Embryonic Development ◽  
Plasma Levels ◽  
Thyroid Stimulating Hormone ◽  
Pituitary Cells ◽  
Hepatic Expression ◽  
Gh Cells ◽  
Igf I

Treatment of fetal rats and embryonic chickens with exogenous glucocorticoids induces premature GH cell differentiation. However, it is unknown whether the developing adrenal gland is capable of mounting this response autonomously. The present study determined whether stimulation of the adrenal gland in developing chicken embryos through administration of ACTH could induce a premature increase in GH cells. We found that plasma corticosterone and ACTH levels increased between embryonic day (e) 11 and e17, consistent with GH cell (somatotroph) ontogeny. Injection of ACTH into eggs on e9, e10, or e11 increased somatotrophs on e14. In contrast, thyroid-stimulating hormone, CRH, α-MSH, GHRH, and TRH were ineffective. Culture of e11 pituitary cells with ACTH failed to induce somatotrophs, suggesting an indirect action of ACTH on GH cells in vivo. Intravenous administration of ACTH dramatically increased plasma levels of corticosterone within 1 h and increased the percentage of pituitary somatotrophs within 24 h. Although ACTH administration increased the relative abundance of pituitary GH cells, there was no effect on plasma levels of GH, IGF-I, or IGF-II, or in hepatic expression of IGF-I or IGF-II mRNA. We conclude that ACTH administration can increase the population of GH cells in the embryonic pituitary. However, this treatment alone does not lead to downstream activation of hepatic IGF production. These findings indicate that the embryonic adrenal gland, and ultimately anterior pituitary corticotrophs, may function to regulate pituitary GH cell differentiation during embryonic development.

GRF treatment of late pregnant ewes alters maternal and fetal somatotropic axis activity

1991 ◽  
Vol 260 (4) ◽  
pp. E575-E580 ◽  
Author(s):  
M. M. Blanchard ◽  
C. G. Goodyer ◽  
J. Charrier ◽  
G. Kann ◽  
R. Garcia-Villar ◽  
...  
Keyword(s):  
Plasma Levels ◽  
Late Gestation ◽  
Placental Lactogen ◽  
Maximal Response ◽  
Pituitary Cells ◽  
In Vitro Test ◽  
Fetal Sheep ◽  
Igf I

To examine the effects of anabolic agents given during late gestation on the maternal and fetal somatotropic axes, we injected pregnant ewes twice daily with 0.15 mg somatocrinin (GRF)-(1-29) for 10 days beginning on day 130 of gestation. Maternal and fetal endocrine changes were compared with control animals using both in vivo and in vitro approaches. Treatment with GRF increased maternal plasma levels of growth hormone (GH) and insulin-like growth factor I (IGF-I;P less than 0.05) but not IGF-II. Under in vitro test conditions, maternal pituitary cells showed a greater maximal response (P less than 0.001) to GRF. In the fetuses of treated ewes, cord plasma GH levels were not significantly increased compared with controls. These animals had similar IGF-I but higher IGF-II (P less than 0.05) plasma levels. The maximal response of fetal pituitary cells to GRF was increased (P less than 0.001). GRF treatment had no influence on maternal and fetal pituitary cell responses to somatostatin under either basal or GRF-stimulated conditions. In addition, these treatments did not affect plasma levels of placental lactogen, glucose, or free fatty acids in the maternal and fetal sheep. These data are compatible with the hypothesis that treatment of pregnant ewes in the last days of gestation with GRF could support accelerated fetal growth.

scholarly journals Pituitary Expression of Type I and Type II Glucocorticoid Receptors during Chicken Embryonic Development and Their Involvement in Growth Hormone Cell Differentiation

Endocrinology ◽  
2004 ◽  
Vol 145 (7) ◽  
pp. 3523-3531 ◽  
Author(s):  
Ioannis Bossis ◽  
Shotaro Nishimura ◽  
Michael Muchow ◽  
Tom E. Porter
Keyword(s):  
Cell Differentiation ◽  
Embryonic Development ◽  
Glucocorticoid Receptors ◽  
Type I ◽  
Pituitary Cells ◽  
Type Ii ◽  
Growth Hormone Cell ◽  
D 12

Abstract Glucocorticoids can induce somatotroph differentiation in vitro and in vivo during chick embryonic and rat fetal development. In the present study, we identified the nuclear receptors involved in somatotroph differentiation and examined their ontogeny and cellular distribution during pituitary development in the chicken embryo. Several steroids were tested for their ability to induce GH cell differentiation. Only glucocorticoids and aldosterone were effective at low nanomolar concentrations, suggesting involvement of both type I (mineralocorticoid) and type II (glucocorticoid) receptors (MR and GR, respectively). ZK98299 and spironolactone (GR and MR antagonists, respectively) when used alone were unable to block corticosterone or aldosterone (2 nm)-induced somatotroph differentiation. However, ZK98299 and spironolactone in combination abolished corticosterone or aldosterone (2 nm)-induced somatotroph differentiation. When used separately, both antagonists attenuated induction of GH mRNA by corticosterone. Spironolactone alone blocked somatotroph differentiation induced by 0.2 nm corticosterone or aldosterone, indicating that corticosteroids at subnanomolar concentrations act only through the MR. GR protein was detected in pituitary extracts as early as embryonic d 8, whereas MR protein was readily detectable only around d 12. GR were expressed in greater than 95% of all pituitary cells, whereas MR were expressed in about 40% of all pituitary cells. Dual-label immunofluorescence revealed that the majority of somatotrophs on d 12 expressed MR. Given the high affinity of corticosteroids for MR and that corticosteroid concentrations during embryonic development are in the subnanomolar range, expression of MR may constitute a significant developmental event during somatotroph differentiation.

scholarly journals Demonstration of in vivo mammogenic and lactogenic effects of recombinant ovine placental lactogen and mammogenic effect of recombinant ovine GH in ewes during artificial induction of lactation

1999 ◽  
Vol 160 (3) ◽  
pp. 365-377 ◽  
Author(s):  
G Kann ◽  
A Delobelle-Deroide ◽  
L Belair ◽  
A Gertler ◽  
J Djiane
Keyword(s):  
Plasma Levels ◽  
Placental Lactogen ◽  
Mammary Tissue ◽  
Control Group ◽  
Dependent Manner ◽  
Exogenous Hormone ◽  
Daily Group ◽  
Igf I ◽  
Beta Casein

The present study demonstrates that ovine placental lactogen (oPL) (ovine chorionic somatotrophin) may have an important role in the mammogenesis and/or lactogenesis of the ewe. Its effects were compared with that already described for ovine growth hormone (oGH). In the first experiment, 40 nulliparous ewes were induced to lactate by means of a 7 day (days 1-7) oestro-progestative treatment (E2+P4). The ewes from Group 1 (n=12) received no further treatment, while those of the other groups received either recombinant oGH (roGH, 28 micrograms/kg, i.m., twice daily, Group 2, n=12) or recombinant oPL (roPL, 79 micrograms/kg, i.m., twice daily, Group 3, n=12) from day 11 to 20. All ewes received 25 mg hydrocortisone acetate (HC) twice daily on days 18-20. Control Group 00 (n=2) received no steroid treatment at all, and the control Group 0 (n=2) received only the E2+P4 treatment. Thirteen ewes (three from each experimental group and the two of each control group) were slaughtered at the end of hormone treatments (day 21) before any milking stimulus. The 27 remaining ewes from Groups 1-3 were machine-milked and milk yields recorded daily from day 21 to 76. The E2+P4 treatment enhanced the plasma levels of oPRL, oGH and IGF-I between days 1 and 7 by 1.5, 2. 3 and 2.6 times respectively (P=0.002); roGH treatment induced a highly significant enhancement of IGF-I plasma levels from day 11 to 20, whereas a similar effect appeared for roPL-treated ewes only from day 17 to 20 (P<0.01). Eight weeks after the last exogenous hormone injections, milk yields of both roGH- and roPL-treated groups progressively rose to twice that of unsupplemented groups (P<0.001). The mammary DNA content on day 21 was higher for animals which received either oGH or oPL but, due to individual variations in so few samples (n=3), this difference was not significant. No beta-casein was measured in mammary tissue from control ewes, whereas steroid-treated ewes (E2+P4+HC) had higher casein concentrations regardless of subsequent hormonal treatment on days 11-20 (P<0.001). beta-Casein concentrations in mammary parenchyma of roGH-treated ewes did not differ from that of ewes which received only E2+P4+HC; roPL supplementation clearly enhanced expression of beta-casein (P<0.001). IGF-I stimulation by either roGH or roPL was more precisely examined during a second experiment, in which two twice-daily i.m. doses (58 or 116 micrograms/kg) of either roGH or roPL were administered to four groups of six ewes that were E2+P4 treated as those of Experiment 1. A control group (n=6) received no exogenous hormone from day 11 to 13. On day 13, hourly blood samples were taken from all ewes over 11 h. Both doses of roGH significantly stimulated IGF-I in a dose-dependent manner. The 58 micrograms/kg dose of roPL did not significantly stimulate IGF-I, but although being somewhat less efficient than the 58 micrograms/kg dose of roGH, the 116 micrograms/kg dose of roPL significantly stimulated IGF-I secretion (P<0. 001). These results suggest that mammogenesis and/or lactogenesis in the ewe is in part controlled by somatotrophic hormones such as oGH and oPL and that IGF-I could be one of the mediators of these hormones.

scholarly journals Thyroid Hormones Interact with Glucocorticoids to Affect Somatotroph Abundance in Chicken Embryonic Pituitary Cells in Vitro

Endocrinology ◽  
2003 ◽  
Vol 144 (9) ◽  
pp. 3836-3841 ◽  
Author(s):  
Lixin Liu ◽  
Carlton E. Dean ◽  
Tom E. Porter
Keyword(s):  
Synergistic Effect ◽  
Thyroid Hormones ◽  
Adrenal Glands ◽  
Normal Development ◽  
Pituitary Cells ◽  
Complex Interactions ◽  
Gh Cells ◽  
Iopanoic Acid

Abstract Our laboratory has reported that somatotroph differentiation occurs between d 14 and d 16 of chicken embryonic development and that corticosterone (CORT) can induce somatotroph differentiation at an earlier age in vitro and in vivo. The objective of the present study was to test for thyroid hormone-CORT interactions on somatotroph differentiation in vitro. Pituitary cells from d 11 chicken embryos were treated with CORT and thyroid hormones, and GH-producing somatotrophs were detected by reverse hemolytic plaque assays and immunocytochemistry. We found that thyroid hormones can act synergistically with CORT to further augment the abundance of somatotrophs in vitro but have little to no effect on their own. Both T4 and T3 could act synergistically with CORT to increase somatotroph abundance, but the effects of T3 were biphasic, inhibiting CORT actions at higher concentrations. The monodeiodination inhibitor iopanoic acid inhibited the synergistic effect of T4 on CORT induction of GH cells in vitro but not the synergistic effect of CORT and T3 or the effect of CORT alone. Furthermore, T3 treatment overcame the iopanoic acid-induced reduction in the T4-CORT effect. Our findings indicate that thyroid hormones act synergistically with CORT to further augment the abundance of somatotrophs in vitro and that conversion of T4 to T3 within the pituitary is involved in T4 modulation of somatotroph abundance. Somatotroph differentiation during normal development may be regulated by complex interactions of hormones produced by the embryonic thyroid and adrenal glands.

Myostatin stimulates myosatellite cell differentiation in a novel model system: evidence for gene subfunctionalization

2012 ◽  
Vol 302 (9) ◽  
pp. R1059-R1066 ◽  
Author(s):  
Dilip K. Garikipati ◽  
Buel D. Rodgers
Keyword(s):  
Rainbow Trout ◽  
Cell Differentiation ◽  
Cell Lines ◽  
Mammalian Cell ◽  
Negative Regulator ◽  
Mammalian Cell Lines ◽  
Igf I ◽  
Marker Expression ◽  
Myosatellite Cells

Myosatellite cells play an important role in mammalian muscle regeneration as they differentiate and fuse with mature fibers. In fish, they also contribute to postnatal growth and the formation of new fibers. The relative conservation of fish systems, however, is not well known nor are the underlying mechanisms that control myosatellite cell differentiation. We therefore characterized this process in primary cells from rainbow trout and determined the effects of two known regulators in mammalian systems: IGF-I and myostatin. Unlike mammalian cell lines, subconfluent and proliferating trout myosatellite cells differentiated spontaneously and at a rate proportional to serum concentration. The expression of key myogenic markers (Myf5, MyoD1, myogenin, and MLC) and of the different myostatin paralogs (MSTN-1a/1b/2a) increased with serum-stimulated differentiation, although MSTN-1a expression was consistently higher than that of the other paralogs. In addition, MSTN-2a was only expressed as an unprocessed transcript. In low serum, where differentiation is normally suppressed, recombinant myostatin stimulated myogenic marker expression over time. The opposite was true for IGF-I as it stimulated proliferation, not differentiation, and additionally antagonized myostatin. This includes myostatin's effects on marker expression and on the autoregulation of MSTN-1a and -1b expression. These results conflict with studies using mammalian cell lines and suggest, alternatively, that myostatin is a positive, not negative, regulator of myosatellite cell differentiation. Mammalian myoblasts differentiate when confluent and with serum withdrawal, which differs considerably from how myosatellite cells differentiate in vivo. Thus the primary rainbow trout myosatellite cell culture system appears to be more physiologically relevant.

Effects of a high-glucose environment on the pituitary growth hormone-releasing hormone receptor: type 1 diabetes compared with in vitro glucotoxicity

2008 ◽  
Vol 294 (4) ◽  
pp. E740-E751 ◽  
Author(s):  
Karine Bédard ◽  
Julie Strecko ◽  
Karyne Thériault ◽  
Julie Bédard ◽  
Christelle Veyrat-Durebex ◽  
...  
Keyword(s):  
High Glucose ◽  
Time Course ◽  
Diabetic Rats ◽  
Pituitary Cells ◽  
Mrna Levels ◽  
Mrna Transcript ◽  
Protein Levels ◽  
Igf I

The present study investigated the effects of diabetes and high glucose on GHRH receptor (GHRH-R) mRNA and protein levels in the pituitary of diabetic rats 2, 21, and 60 days post-streptozotocin (post-STZ) administration. Two days post-STZ, the 2.5-kb GHRH-R mRNA transcript was increased. Twenty-one days post-STZ, both the 2.5- and 4-kb transcripts and a 72-kDa 125I-GHRH-GHRH-R complex were elevated. Sixty days post-STZ, the 4-kb transcript remained increased and the 45-kDa 125I-GHRH-GHRH-R complex (functional receptor) was decreased. Hypothalamic GHRH mRNA and serum total IGF-I levels were reduced at all three time points. To better understand the role of high glucose on GHRH-R regulation, time-course effects of 33 compared with 6 mM d-glucose (DG) were examined in cultured anterior pituitary cells from 2-mo-old healthy rats. Membrane lipoperoxidation was present in 33 mM DG, and GHRH-R mRNA levels were diminished after 24 h, Fluo-GHRH internalization was marginal after 16–24 h, and GHRH-induced cAMP levels were decreased after 24 and 48 h. Altogether, these results indicate that the increase of the 2.5-kb GHRH-R mRNA transcript in vivo could be a consequence of a decrease of hypothalamic GHRH mRNA levels in STZ rats. Since it does not affect primarily functional GHRH-R levels, the initial diminution of circulating IGF-I levels could result from a decreased GHRH-R stimulation by GHRH. Thus, the effect of glucotoxicity would be related to a decrease of functional GHRH-R protein, as observed in rats 60 days post-STZ and in cultured pituitary cells from healthy rats exposed to a high-glucose environment.

Plasma levels of bradykinin are suppressed in factor XII-deficient mice

2006 ◽  
Vol 95 (06) ◽  
pp. 1003-1010 ◽  
Author(s):  
Takayuki Iwaki ◽  
Francis Castellino
Keyword(s):  
Embryonic Development ◽  
Plasma Levels ◽  
Factor Xii ◽  
Male And Female ◽  
Adult Mice ◽  
Artificial Surface ◽  
Neomycin Resistance ◽  
Dependent Pathway ◽  
Deficient Mice

SummaryA genetically-transmissible factor (F) XII-inactivated allele has been produced in mice by targeted replacement of exons 3–8 of the FXII gene with the neomycin resistance gene. Interbreeding of these mice provided offspring homozygous for two inactivated FXII alleles (FXII−/−). Male and female FXII-deficient mice bred normally in all genotypic combinations of the heterozygous and homozygous states, and the offspring survived to adulthood, suggesting that a total FXII deficiency does not affect embryonic development and survival. Neither FXII transcripts nor FXII antigen was found in various tissues of adult FXII−/−mice. No obvious unchallenged coagulopathies were present in FXII−/−adult mice, despite greatly prolonged activated partial thromboplastin times in this mouse cohort. FXII−/−mice were then used to assess the in vivo importance of the plasma FXII/prekallikrein/kininogen pathway in provision of resting plasma bradykinin (BK) levels and in generation of plasma BK stimulated by contact with an artificial surface, using a new and greatly improved plasma BK assay developed during these studies. It was found that approximately 50% of resting BK, and all of the contact-stimulated plasma BK, was provided by this FXII-dependent pathway, without a requirement for FXI. These results provide clear evidence that surface-stimulated BK production, in mice, is dependent on the activation of FXII.

scholarly journals Evidence that lactotrophs do not differentiate directly from somatotrophs during chick embryonic development

2004 ◽  
Vol 183 (2) ◽  
pp. 417-425 ◽  
Author(s):  
Xiaoqin Fu ◽  
Shotaro Nishimura ◽  
Tom E Porter
Keyword(s):  
Growth Hormone ◽  
Embryonic Development ◽  
Anterior Pituitary ◽  
Intermediate Cell ◽  
Pituitary Cells ◽  
Cell Type ◽  
Caudal Lobe ◽  
Pituitary Development ◽  
Gh Cells ◽  
Cephalic Lobe

It is generally accepted that, in mammals, lactotrophs differentiate from somatotrophs through an intermediate cell type, the mammosomatotroph. However, little information exists about mammosomatotrophs and their relationship with lactotroph development in non-mammalian vertebrates. We reported previously that corticosterone (CORT) can induce both somatotroph and lactotroph differentiation in cultures of chicken embryonic pituitary cells. Our current objectives were to determine the abundance of mammosomatotrophs during chicken pituitary development, to identify mammosomatotrophs during CORT induction of lactotrophs, and to explore whether lactotrophs induced by CORT are derived from somatotrophs. Cells that produced prolactin (PRL) only, growth hormone (GH) only or both hormones simultaneously were detected by three approaches – dual immunofluorescence, a combination of immunofluorescence and immunocytochemistry (ICC), and by ICC using combinations of antibodies to GH and PRL. Mammosomatotrophs were not detected between embryonic day (E) 16 and E20, even though lactotrophs increased from nearly absent to greater than 10% of all pituitary cells during this period. CORT induced more than 10% of all E13 pituitary cells to produce PRL, while the percentage of mammosomatotrophs remained at less than 1% of all cells. When cells from the cephalic and caudal lobes of the anterior pituitary were treated separately, CORT increased GH cells in cultures from the caudal lobe. No PRL cells were found in the caudal lobe. In the cephalic lobe, CORT increased lactotrophs, while GH cells were barely detected. In summary, mammosomatotrophs are rare during chicken pituitary development, and CORT does not induce lactotrophs from somatotrophs. These findings indicate that, unlike in mammals, lactotrophs do not differentiate from somatotrophs during chicken embryonic development.

scholarly journals IGF-I enhances cortisol secretion from guinea-pig adrenal gland: in vivo and in vitro study

2007 ◽  
Author(s):  
Dipali Raha ◽  
Shamshun Nehar ◽  
Bhola Paswan ◽  
Piera Rebuffat ◽  
Giuliano Neri ◽  
...  
Keyword(s):  
Adrenal Gland ◽  
Guinea Pig ◽  
In Vitro Study ◽  
Vitro Study ◽  
Cortisol Secretion ◽  
Igf I

Responsiveness of chicken embryonic somatotropes to somatostatin (SRIF) and IGF-I

1997 ◽  
Vol 154 (2) ◽  
pp. 303-310 ◽  
Author(s):  
M M Piper ◽  
T E Porter
Keyword(s):  
Embryonic Development ◽  
Anterior Pituitary ◽  
Pituitary Cells ◽  
Gh Secretion ◽  
Anterior Pituitary Cells ◽  
Igf I

Abstract We have previously demonstrated that chicken embryonic somatotropes are responsive to GHRH shortly after they differentiate. In contrast, relatively little is known about the regulation of GH secretion by somatostatin (SRIF) and IGF-I during chicken embryonic development. In the present study, anterior pituitary cells were isolated from day 16, 18 and 20 embryos and subjected to reverse hemolytic plaque assays (RHPAs) for chicken GH to assess the effect of SRIF and IGF-I on basal GH release and SRIF on GHRH-stimulated GH secretion. We found that all three ages responded to SRIF, under both basal and stimulated conditions. SRIF inhibition of basal GH release was evident for day 18 and 20 cells by 9 h, while 18 h were required for day 16 cells. After 18 h, 10−11 m SRIF depressed basal GH secretion by day 16 and 18 cells, while 10−9 m SRIF was required to depress GH plaque percentages by day 20 cells. GHRH stimulated GH release from all ages tested. After 2 h, SRIF partially suppressed GHRH-stimulated GH release by day 20 cells. After 6 h, day 18 cells responded to SRIF, reducing the percentage of plaque-forming cells under GHRH stimulated conditions. After 18 h, the percentage of day 16 cells forming GH plaques was reduced for cells treated with GHRH and SRIF, compared with cells treated with GHRH alone. All ages examined also responded to IGF-I. After 36 h, GH release by day 16 and 18 cells was decreased when exposed to IGF-I. While IGF-I decreased the relative amount of GH secreted per somatotrope on day 20, a paradoxical increase in the percentage of cells secreting GH was noted. These results indicate that anterior pituitary somatotropes are responsive to SRIF and IGF-I during late embryonic development of chickens. Journal of Endocrinology (1997) 154, 303–310

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