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1.
The effect of vasoactive intestinal peptide (VIP) on prolactin (PRL) secretion from pituitary cells is reviewed and compared to the effect of thyrotropin releasing hormone (TRH). These two peptides induced different secretion profiles from parafused lactotrophs in culture. TRH was found to increase PRL secretion within 4 s and induced a biphasic secretion pattern, while VIP induced a monophasic secretion pattern after a lag time of 45–60 s.The secretion profiles are compared to changes in adenylate cyclase activity, production of inositol polyphosphates, changes in intracellular calcium concentrations and changes in electrophysiological properties of the cell membrane.Abbreviations AC adenylate cyclase - DG diacyglycerol - GH growth hormone - GTP guanosine trisphosphate - Gi GTP binding proteins that mediate inhibition of adenylate cyclase and that are pertussis toxin sensitive - Gs GTP binding protein that mediates stimulation of adenylate cyclase - GH cells clonal rat pituitary tumor cells producing PRL and/or growth hormone - GH3 GH4C1 and GH4B6 subclones of GH cells - PKA protein kinase A - PKC protein kinase C - PLC phospholipase C - PRL prolactin - TPA 12-O-tetradecanoyl phorbol 13-acetate - TRH thyrotropin releasing hormone - VIP vasoactive intestinal peptide  相似文献   

2.
Summary We previously documented both the spontaneous acceleration of growth hormone (GH) and prolactin (PRL) production by GH3 cells during periffusion and the suppression of their production during plate culture. We here present the role played by medium flow itself in this differential behavior. Increasing rates of perifusion flow (pump rates of 1 to 5 ml/h, equivalent to chamber flow rates of 0.19 to 1.3 μl·min−1·mm−2 of cross-sectional area) were associated with enhanced GH and PRL secretion. Flow rate-dependent basal hromone secretion rates were established quickly and were stable for the first 10 to 14 h of perifusion. The previously documented independent, spontaneous, and continuously accelerating production of both hormones that followed during the subsequent 40 (PRL) to 60 (GH) h of perifusion was also shown to be flow-rate related. Any time the rate of medium flow was changed within an experiment, the rate of hormone secretion was modulated. However, that modulation did not interrupt ongoing flow-associated acceleration of hormone production once the latter had begun. In addition, GH3 cell product(s) from one cell column reversibly inhibited secretion from cells in a downstream column. The inhibition did not occur when cells in the downstream column had been exposed to trypsin. Other work had suggested that neither GH, PRL, insulinlike growth factor-I, leucine, nor nutrient exhaustion were responsible for the effect. These data are consistent with autocrine-paracrine feedback regulation of GH3 cells by a secretory product(s). Feedback would thus provide a mechanism to effect flow-rate-dependent modulation of GH and PRL release, and to explain accelerating hormone production during perifusion. This work was supported by a grant to M. E. S. from the National Institutes of Health (DK33388), Bethesda, MD, and in part, by the Medical Research Service of the Veterans Administration.  相似文献   

3.
Summary The secretion of prolactin is increased by treatment of prolactin producing rat pituitary cells with the hypothalamic tripeptide thyroliberin. To investigate the underlying mechanisms we used three closely related rat pituitary tumor cell strains (GH12C1, GH3 and GH4C1), which synthesize and spontaneously secrete prolactin and/or growth hormone. Growth hormone and prolactin released into the culture medium over a period of 24 h were measured by radioimmunoassay. Initial rates of synthesis were measured by immunoprecipitation of intracellular growth hormone and prolactin after incubation of cell cultures with 3H-leucine. The observed increase in prolactin synthesis and release was correlated with morphological effects of thyroliberin treatment. The volume density of Golgi complexes and the volume and surface densities of rough endoplasmic reticulum were compared in untreated cells and thyroliberin treated cells. As normal distribution could not be assumed, the non-parametric rank test of Wilcoxon was used whereby the densities calculated for each cell section were ranked. Alle three morphological parameters increased after thyroliberin treatment in cells secreting prolactin only (GH4C1), implying that the increase of prolactin secretion, at lest in part, is due to increased prolactin synthesis.  相似文献   

4.
Summary Chronic treatment (more than 3 d) of GH3 cells, cloned rat pituitary cells producing prolactin, with 100 nM TRH resulted in a 41% reduction in the rate of cell growth in a medium containing 0.5% fetal bovine serum. These effects of TRH appeared both in the medium containing a higher concentration of serum and in that containing six growth factors, i.e. insulin, transferrin, parathyroid hormone, fibroblast growth factor, triiodothyronine, and multiplication-stimulating activity (MSA) instead of serum. TRH stimulated prolactin production by GH3 cells in a dose-dependent manner both in the serum-supplemented and serum-free media. On the other hand, TRH, at 1 nM, elicited a 130% stimulation in the cellular growth, whereas, at concentrations of more than 10 nM, it inhibited the growth significantly. In the defined culture system, it was demonstrated that TRH stimulated prolactin production in the presence or absence of six growth factors, whereas its inhibitory effects on cellular growth appeared only in the presence of MSA regardless of the presence or absence of the other five factors. Furthermore, it was shown that a dose-dependent stimulatory effect of MSA on the growth of GH3 cells was suppressed by TRH. TRH exhibited only a stimulatory effect on cellular growth in the medium containing the five factors other than MSA. In conclusion, TRH could inhibit cell growth of GH3 in the presence of MSA in the defined medium or MSA-like factor(s) in the serum-supplemented medium.  相似文献   

5.
Summary GH cells are a widely used cell strain for the investigation of mechanisms regulating hormone release and synthesis. This report identifies two inducible phenotypes of the GH4 clone (epithelioid and motile) which may extend studies of this well-characterized cell line to different stages of pituitary cell development. GH4C1 cells treated in suspension with epidermal growth factor plus tetradecanoylphorbol acetate aggregate to form large epithelioid colonies with extensive cell-to-cell and cell-to-substratum adhesion. These cells cease replicating within 48 h, increase 50% in cell volume, and synthesize 40-fold more prolactin. A GH4C1 variant with enhanced substratum adhesion and little or no cell-to-cell adhesion (GH4S1), responds differently to this treatment. These cells cease replicating immediately, show increased cell separation, develop leading lamellae, and display locomotory activity. Each phenotype coexists in mixed cultures of GH4C1 and GH4S1 cells. This indicates that the different inducible response of the variant does not result from autocrine secretion. A molecular basis for cell-to-cell adhesion in GH4 cells was investigated. GH4C1, but not the variant cells, express a 180 kDa immunoreactive protein indistinguishable from an isoform of the neural cell adhesion molecule. Therefore the absence of cell-to-cell adhesion and inability to develop extensive cell-to-cell adhesion characteristic of the epithelioid phenotype may result from altered expression of the neural cell adhesion molecule. These findings are important because they have defined an in vitro approach to investigate genetic and cellular changes associated with the development and progression of pituitary cell phenotype. This study was initiated in the laboratory of Dr. A. H. Tashjian, Jr., under the support of grant DK11011 from the National Institutes of Health, Bethesda, MD. The completion of this study was supported by the Medical University of South Carolina Biomedical Support Grant of 1987–1988 and the American Cancer Society grant 1N-175.  相似文献   

6.
The effects of colchicine and 2-Br-α-ergocryptine-methane-sulfonate (CB 154) on the release of prolactin and growth hormone have been studied in a clonal strain of rat pituitary tumor cells (GH3) in monolayer culture. These cultures produce both prolactin and growth hormone and release both proteins spontaneously into the medium without storing them in large amounts. Immunological methods were used to measure both intracellular and extracellular concentrations of the hormones. Colchicine (5 × 10?6 M for 3 hours) caused a 2- to 3-fold increase in intracellular concentrations of prolactin and growth hormone but, under basal conditions, had little or no measurable effect on the amounts of hormone accumulated in the medium during the course of the standard three hour treatment period. This latter finding evidently is due to a lag in the onset of drug action. Colchicine had little or no effect on accumulation of extracellular prolactin during the first two hours of treatment whereas such accumulation was depressed by over 60% during the third hour of treatment. Previous studies have shown that treatment of GH3 cells with thyrotropin releasing hormone (TRH) and hydrocortisone (HC) increases both intra and extracellular levels of prolactin and growth hormone, respectively. In cultures treated with TRH (5 × 10?8 M), colchicine (5 × 10?6 M for 3 hours) increased intracellular prolactin by about 70% and decreased extracellular hormone by 10%. In cultures treated with HC (3 × 1O?6 M), colchicine increased intracellular growth hormone by more than 100% and decreased medium concentrations of the hormone by 15%. Colchicine did not significantly alter total hormone (intracellular + extracellular) accumulation, cellular uptake of 3H-amino acids, or total cell protein synthesis. The synthetic ergot alkaloid, CB 154, (3.3 × 10?6 M for 3 hours) caused an 80% increase in intracellular, and a nearly 50% decrease in extracellular, prolactin without affecting the accumulation of growth hormone, the uptake of 3H-labeled amino acids, or overall protein synthesis in the cultures. Elevation of medium potassium concentration from a basal value of 5.3 mM to 3–5 × 10?2 M (by addition of KCl) decreased intracellular levels of prolactin by 85% and growth hormone by 55%. These effects of high potassium were blocked by colchicine and by CB 154. We conclude that colchicine, after a lag period of two hours, acts to inhibit the release of prolactin and growth hormone from GH3 cells. By the end of three hours of treatment, this inhibition is over 60% complete in the case of prolactin. The qualitatively different effects of colchicine and CB 154 on prolactin and growth hormone release suggest that these two secretory blocking agents probably act on GH3 cells by different mechanisms.  相似文献   

7.
Summary The rates at which growth hormone (GH) and prolactin (PRL) are spontaneously secreted from a rat pituitary tumor cell line (GH3) were significantly reduced when these cells were maintained in medium containing 2.5 μg/ml Fungizone (Fz). The reduction in hormone secretion was not immediately reversed by removal of Fz during perifusion, but after 3 wk in control medium, secretory rates approached the pre-Fz treatment levels. In plated cells, secretion of GH was reduced by Fz in a dose-dependent manner, whereas PRL secretion was significantly reduced only by the highest concentration (2.5 μg/ml) of Fz. We concluded that Fz is not an acceptable medium constituent for the long-term culture of GH3 cells. However, because its effects are reversible, its short-term use as a decontaminating agent might eliminate the necessity for reinitiating the culture of cells whose secretory behavior must be followed in long-term protocols. Technical assistance provided by Y. S. Lee. Supported by grant AM33388 to M. E. S. from the National Institutes of Health, Bethesda, MD, and in part by the Medical Research Service of the Veterans Administration.  相似文献   

8.
Summary In previous work we have shown that perifused GH3 cells exhibit spontaneously accelerating growth hormone (GH) and prolactin (PRL) secretory rates. This behavior contrasts with GH and PRL secretion rates that are decreasing or stable over the same 3-d period in static cell culture. We now report that GH3 cells maintained in serum-supplemented medium produce an autocrine-paracrine factor(s) which inhibits GH secretion in plate culture; PRL release is frequently reduced as well. The inhibitory effect of conditioned medium on GH secretion was concentration dependent, whereas PRL release was stimulated at low and inhibited at high concentrations over the same range. Extensive dialysis of conditioned medium using membranes with a molecular weight cut-off of 12 000–14 000 did not remove GH inhibition but produced a retentate that stimulated PRL secretion. Heat-inactivation of conditioned medium did not abolish inhibition of GH release but did remove the PRL-stimulatory effect. IGF-I added to fresh culture medium did not reproduce the GH-inhibitory effects of conditioned medium. We conclude that GH3 cell secretory behavior in perifusion and plate culture systems may be partially explained by the production of an autocrine-paracrine factor: its accumulation in plate culture inhibits GH and PRL secretion whereas its removal, by perifusing medium, allows GH and PRL secretion to accelerate. Supported by grant DK33388 to M. E. S. from the National Institute of Health, Bethesda, MD, and in part by the Medical Research Service of the Veterans Administration, Washington, DC.  相似文献   

9.
10.
The present study was undertaken to investigate the effects of selenite (SeIV) and selenate (SeVI) on the all-trans retinoic acid (RA)-nuclear retinoic acid receptor (RAR) complex formation in rat liver. We also present the data on the in vitro effects of SeIV on the RARα and the type I iodothyronine 5′-deiodinase gene expression in the GH4C1 rat pituitary tumor cells. SeIV at 1.0 μmol/L was found to reduce (p<0.05) the RA specific binding to RAR in rat liver. Dithiothreitol (DTT), a protective agent for sulfhydryl groups, was found to be slightly effective in protecting the RAR binding properties when affected by SeIV. SeVI at 0.1 μmol/L reduced (p<0.05) the RA specific binding to RAR in liver, as well. Seleno-l-methionine (Se-II) when compared tol-methionine did not exert any inhibitory effect on the formation of the RA-RAR complex. SeIV (up to 2.5 μmol/L) has no inhibitory effect on GH4C1 cell proliferation as well as the prolactin secretion. SeIV at 1.0 μmol/L significantly decreases the rate of mRNA synthesis and/or degradation of the α form of the RAR and causes the enhancement of the type I iodothyronine 5′-deiodinase gene expression in GH4C1 cells. The results based on in vitro experiments suggest that inorganic selenium may affect the RA specific binding to their cognate receptor molecules, and it may reduce expression of the gene encoding the RARα, with the cell vitality and the cell growth remaining unchanged.  相似文献   

11.
Prolactin and growth hormone production were measured in a rat pituitary tumour cell strain (GH3) after treatment with cortisol (5 × 10?6 M), thyroliberin (2.5 × 10?6 M) and 17β-estradiol (10?6 M). The changes in hormone production were related to alterations in cell growth rate and cell cycle distribution. Cortisol inhibited prolactin production, stimulated growth hormone production and reduced the cellular growth rate measured two days after start of treatment (maximum about 40% inhibition). Flow-micro fluorometric analysis of DNA distributions showed that cortisol treatment reduced the relative number of cells in S phase (maximum effect about 50%) with a compensatory increase of the proportion of cells in G1 phase. The lack of inhibition of prolactin production after three days of cortisol treatment may partly be related to the increased number of cells in G1 phase. Thyroliberin and 17β-estradiol did not significantly affect cell growth after six days of treatment, although the fraction of cells in S phase was reduced by approximately 40% with a corresponding increase of cells in G1 phase. For thyroliberin and 17β-estradiol, the stimulatory effect on prolactin production and the inhibitory effect on growth hormone production witin a period of treatment of six days cannot be explained by a shift in cell cycle distributions. None of the three hormones influenced the growth fraction which was equal to unity. In conclusion, thyroliberin and 17β-etradiol are able to change prolactin and growth hormone production without altering the cell cycle distribution. However, the effects of cortisol on prolactin and growth hormone production may partly be due to an alteration in cell cycle traverse resulting in an increased number of cells in the G1 phase.  相似文献   

12.
Cholecystokinin-octapeptide (CCK-8)(10?6 to 10?8M) produced a marked increase in growth hormone (GH) release from incubated rat anterior pituitary quarters and from cultured GH3 pituitary tumor cells. Although several CCK-8 analogues also caused GH release, bombesin, secretin and pancreatic polypeptide had no effect on GH secretion in vitro. In the GH3 cell line, CCK-8 (10?7M) reversed the inhibitory effect of somatostatin (10?5M) on GH release. As CCK immunoreactivity has been demonstrated to be present in the hypothalamus, these results suggest that CCK-8 may be a physiologically important growth hormone releasing factor.  相似文献   

13.
D K Biswas  J Lyons  A H Tashjian 《Cell》1977,11(2):431-439
The clonal strain of pituitary tumor cells GH12C1 does not produce detectable amounts of prolactin (<5 ng/mg cell protein per 24 hr), although it does synthesize growth hormone. When GH12C1 cells were grown in the presence of 5-bromodeoxyuridine (BrdU, 3 μg/ml), the cells did produce prolactin as determined by quantitative microcomplement fixation and incorporation of 3H-leucine into 3H-prolactin. BGH12C1 and F1BGH12C1, two BrdU-resistant (r) substrains derived from GH12C1 which grow in the presence of 30 μg/ml BrdU, also synthesized prolactin (100–500 ng/mg cell protein per 24 hr). Growth of BrdUr strains was not dependent upon on the presence of the drug in the medium; however, the continued production of prolactin by F1BGH12C1 cells was dependent upon the presence of BrdU. Growth hormone production in both BrdUs and BrdUr strains was not affected by BrdU. Resistance of F1BGH12C1 cells to BrdU was not due to a defect in BrdU uptake. Thymidine inhibited the incorporation of 3H-BrdU into DNA in both sensitive and resistant strains, and also reduced BrdU-induced prolactin synthesis in F1BGH12C1. We postulate that induction of prolactin synthesis by BrdU in GH12C1 and F1BGH12C1 cells is mediated by the incorporation of the drug into cellular DNA. Furthermore, the lack of measurable prolactin synthesis by the parent strain GH12C1 is not due to deletion of the gene for prolactin, but is probably the result of regulatory mechanisms which do not permit expression of this gene.  相似文献   

14.
Summary The artificial sweetener saccharin inhibits binding of epidermal growth factor (EGF) to cultured rat pituitary tumor cells (GH4C1 cells). Saccharin also causes morphological alterations in these cells, resulting in pronounced elongation, stretching, and firmer attachment of cells to the culture dishes. These alterations in cell shape are similar to those observed after treatment of GH4C1 cells with EGF and with thyrotropin-releasing hormone (TRH), both of which enhance prolactin (PRL) production in these cells. After assaying for PRL in saccharin-treated cultures, it was observed that this sweetener is also capable of stimulating PRL production two-to sixfold in a dose-dependent manner. Enhancement of PRL production can be observed at 0.5 mM saccharin, yet this is 10 times less than the saccharin concentration required to alter cell shape. These effects of saccharin on cell morphology and on PRL production are reversible in GH4C1 cell cultures. When added to cultures along with maximal concentrations of EGF or TRH, the effects of saccharin on PRL production are additive, suggesting that the actions of saccharin are mediated by a somewhat different pathway from that of the peptide hormones. Pulse labeling studies indicate that the enhancement of PRL production is highly specific inasmuch as saccharin was found to decrease the overall rate of protein synthesis in these cells. Saccharin also causes a decrease in the rate of DNA synthesis under these treatment conditions. Mitomycin C, which similarly inhibited DNA synthesis, had no effect on cell morphology or PRL production. This investigation was supported by a Faculty Research Grant from Wheaton College  相似文献   

15.
Summary GH3 cell secretory activity was studied in long-term perifusion to define previously reported spontaneous increases in growth hormone (GH) and prolactin production (PRL). Mechanically harvested cells (1×107/column) were perifused at 4 ml/h for 72 h. A basal period of variable duration (8 to 12 h), during which hormone secretion was stable, was followed by steadily increasing secretion rates. Changes in cell number were not sufficient to acount for increased jormone secretion rates: a) there was no significant change in cell count after 72 h (0.97±0.03×107;n=18); b) mean cell column DNA content increased 25.5% above the base value, whereas GH secretion rose 385% and PRL rose 178% (n=5). Observed differences in the duration of the basal secretion period, the basal secretory rate, and the magnitude of secretory rate increase were associated with several variables: a) variablility within a subline was a function of passage number: GH secretion decreased and PRL secretion increased with subculture number; b) cells with identical lot and freeze numbers, but received at different times, behaved differently; c) the presence of an antifungal agent (nystatin) altered hormone secretion reproducibly. Conclusions: a) rates of GH and PRL secretion rise spontaneously in perifusion without a proportional increase in GH3 cell number; b) fluctuations in the rate of GH3 cell secretion of GH and PRL are not entirely random but are determined by several definable variables. Supported by a grant to MES from the National Institutes of Health (AM33388) and in part by the Medical Research Service of the Veterans Administration.  相似文献   

16.
Primary cultures containing a high percentage of lactotrophs were obtained by dissociating the pituitary of rats following 14–18 days of lactation. Lactotrophs with a distinctive appearance were recorded after 1–35 days in vitro and identified by immunocytochemical staining for prolactin. Whole-cell voltage clamp measurements in isotonic KCl solution from a holding potential of −40 mV revealed the presence of inward-rectifying K currents with a time-dependent, Na+-independent inactivation at potentials negative to −60 mV. The time for complete inactivation was strikingly different between lactotrophs, varying between 1 sec and more than 5 sec at −120 mV, and was not related to time in culture. The reversal potential shifted 59 mV (25°C) for a tenfold change in external K+ concentration, demonstrating the selectivity of the channel for K+ over Na+. The inward-rectifying K current was blocked by 5 mm Ba2+ and partially blocked by 10 mm TEA. Chloramine-T (1 and 2 mm) produced a total block of the inward-rectifying K current in lactotrophs. Thyrotropin-releasing hormone (500 nm) significantly reduced the inward-rectifying K current in about half of the lactotrophs. This current is similar to the inward-rectifying K current previously characterized in clonal somatomammotrophic pituitary cells (GH3B6). The variability of the rate of inactivation of this current in lactotrophs and its responsiveness to TRH is discussed. Received: 28 September 1995/Revised: 11 December 1995  相似文献   

17.
Intracellular location of newly synthesized growth hormone   总被引:4,自引:0,他引:4  
The current model for the synthesis and secretion of protein hormones by cells of the anterior pituitary leads to a prediction that newly synthesized GH should be membrane-associated. Experiments were performed to test this prediction. Rat pituitary tumor cells (GH3) were pulsed with 3H-leucine for 2 min, and chased with cold leucine for min. Analysis of subcellular fractions by SDS polyacrylamide gel electrophoresis and by immunoprecipitation of GH demonstrated that most (86%) of the newly synthesized GH is membrane-associated.  相似文献   

18.
The object of the present study was to determine the relative importance of Ca++ and cyclic nucleotides as “second messengers” in thyroliberin (TRH)-mediated prolactin (PRL) release in the GH3 and GH4 rat pituitary tumor cell lines. PRL, cyclic adenosine 3': 5'-monophosphate (cAMP), and cyclic guanosine 3': 5'-monophosphate (cGMP) were measured by radioimmunoassay (RIA) following TRH stimulation. TRH increased PRL release and cAMP levels in GH3 and GH4 cells, but cGMP increases were variable. Treatment with 1 mM theophylline increased PRL release and raised cAMP and cGMP. Addition of TRH to theophylline-pretreated cells produced further significant increases in PRL release without any additional increases in cAMP and cGMP. Co++, a Ca++ antagonist, abolished TRH-induced PRL release in a dose-dependent manner. The Co++ inhibition was partially reversed by Ca++ in GH3 or GH4 cells. Furthermore, the Ca++ ionophore A23187 stimulated PRL release. We conclude that Ca++ is the primary “second messenger” for TRH-mediated PRL release from GH3 or GH4 cells.  相似文献   

19.
ATP-sensitive K+ (KATP) channels have been characterized in pituitary GH3 cells with the aid of the patch-clamp technique. In the cell-attached configuration, the presence of diazoxide (100 μm) revealed the presence of glibenclamide-sensitive KATP channel exhibiting a unitary conductance of 74 pS. Metabolic inhibition induced by 2,4-dinitrophenol (1 mm) or sodium cyanide (300 μm) increased KATP channel activity, while nicorandil (100 μm) had no effect on it. In the inside-out configuration, Mg-ATP applied intracellularly suppressed the activity of KATP channels in a concentration-dependent manner with an IC50 value of 30 μm. The activation of phospholipase A2 caused by mellitin (1 μm) was found to enhance KATP channel activity and further application of aristolochic acid (30 μm) reduced the mellitin-induced increase in channel activity. The challenging of cells with 4,4′-dithiodipyridine (100 μm) also induced KATP channel activity. Diazoxide, mellitin and 4,4′-dithiodipyridine activated the KATP channels that exhibited similar channel-opening kinetics. In addition, under current-clamp conditions, the application of diazoxide (100 μm) hyperpolarized the membrane potential and reduced the firing rate of spontaneous action potentials. The present study clearly indicates that KATP channels similar to those seen in pancreatic β cells are functionally expressed in GH3 cells. In addition to the presence of Ca2+-activated K+ channels, KATP channels found in these cells could thus play an important role in controlling hormonal release by regulating the membrane potential. Received: 19 June 2000/Revised: 13 September 2000  相似文献   

20.
A receptor with specificity and high affinity for hydrocortisone (HC) has been found in the cytosol of GH3 cells, a growth hormone (GH) producing culture. Scatchard analysis indicated that the interaction of [3H]HC with the receptor has an apparent dissociation constant (Kd) of about 6.0 × 10?9M and a concentration of binding sites of approx. 1 × 10?13 mol/mg cytosol protein. The second order association rate constant was determined to be 1.5 × 106 M?1 min?1. The receptor activity is stable at 2°C for several hours, but is destroyed completely by heating at 37°C for 1 hour, or by treatment with pronase, only partially by RNase, but not by DNase. The binding of [3H]HC to the cytosol receptor is inhibited by unlabeled progesterone (PR) or dexamethasone to the same extent as the inhibition by unlabeled HC. However, it is only partially inhibited by testosterone, 17-methyl-testosterone, 17α and 17β-estradiol, and 4-pregnen-20β-ol-3-one, and is unaffected by 5α-pregnan-3β,20β-diol. The biological role for these receptors in the regulation of GH synthesis is supported by the observations that the HC-stimulated production of GH is antagonized by PR, which competes with the binding of HC to the receptor.  相似文献   

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