Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of extracellular Ca2+ in pituitary hormone release was studied in primary cultures of rat anterior pituitary cells. The basal levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), thyrotropin (TSH), and adrenocorticotropin (ACTH) secretion were independent of extracellular Ca2+ concentration ([Ca2+]e). In contrast, the basal levels of growth hormone (GH) and prolactin (PRL) release showed dose-dependent increases with elevation of [Ca2+]e, and were abolished by Ca2+-channel antagonists. Under Ca2+-deficient conditions, BaCl2 mimicked the effects of calcium on PRL and GH release but with a marked increase in potency, and also increased basal LH and FSH release in a dose-dependent manner. In the presence of normal [Ca2+]e, depolarization with K+ maximally increased cytosolic [Ca2+] ([Ca2+]i) from 100 to 185 nM and elevated LH, FSH, TSH, ACTH, PRL, and GH release by 7-, 5-, 4-, 3-, 2-, and 1.5-fold, respectively. These effects of KCl were abolished in Ca2+-deficient medium or in the presence of the Ca2+-channel antagonist, Co2+, and were diminished by the dihydropyridine Ca2+-channel antagonist, nifedipine. The Ca2+-channel agonist BK 8644 (100 nM) enhanced the hormone-releasing actions of 25 mM KCl upon PRL, LH, FSH, GH, TSH, and ACTH by 2.3-, 2.0-, 1.8-, 1.7-, 1.6-, and 1.4-fold, respectively. The dose- and voltage-dependent actions of BK 8644 were specific for individual cell types; BK 8644 enhanced GH, PRL, TSH, LH, and ACTH secretion in the absence of any depolarizing stimulus, with ED50 values of 8, 10, 150, 200, and 400 nM, respectively. However, in the presence of 50 mM KCl, the ED50 values for BK 8644 were 1.5, 2, 3, 5, and 7 nM for GH, PRL, ACTH, TSH, and LH, respectively. [3H]BK 8644 bound specifically to pituitary membranes with Kd values of 0.8 nM and concentrations of about 900 channels per cell. These observations provide evidence for the presence and participation of voltage-sensitive calcium channels in the secretion of all five populations of anterior pituitary cells.
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PMID:Participation of voltage-sensitive calcium channels in pituitary hormone release. 245 42

Normal human melanocytes, unlike malignant melanoma cells, required at least three growth-promoting agents, i.e., phorbol ester for protein kinase C activation and the growth factors basic fibroblast growth factor (bFGF) and insulin, for growth in chemically defined W489 medium. Cell growth was further stimulated by addition of agents that increase intracellular levels of cyclic adenosine 3',5'-monophosphate (cAMP) to the medium. Among these agents, the pituitary hormones alpha-melanocyte-stimulating hormone (alpha-MSH) and follicle-stimulating hormone were the most potent, whereas bacterial toxins, including cholera, tetanus, and pertussis toxin and their subunits either were less mitogenic or gave variable results depending on the culture tested. Medium containing phorbol ester PMA, growth factors bFGF and insulin (or insulin-like growth factor-I), and synthetic alpha-MSH supported melanocyte growth for more than 5 months with doubling times between 5 and 8 days. Two copper-binding proteins, ceruloplasmin and tyrosinase, were mitogenic when added to medium and ceruloplasmic induced a long bi- to tripolar-shape of cells. Addition of 1 mM dibutyryl cAMP to the medium led to the formation of dendrites in all cells, with an average of 28 extensions per cell. Although cell growth was inhibited by dibutyryl cAMP, cells were not terminally differentiated and continued to proliferate. Dendritic melanocytes showed a 2.2-fold increase in activity of the tyrosine kinase pp60c-src. The induction of dendritic processes in melanocytes by dibutyryl cAMP or sodium butyrate was reversible and appears to reflect the expression of the mature melanocytic phenotype in situ.
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PMID:Regulatory factors that determine growth and phenotype of normal human melanocytes. 246 9

To determine whether corticotropin-releasing hormone (CRH) exerts an inhibitory action on gonadotropin secretion in normal fertile women, the effects of CRH on luteinizing hormone (LH), follicle-stimulating hormone (FSH), and cortisol secretion were studied during the menstrual cycle. CRH had no effect on LH release during the midfollicular phase of the cycle. By contrast, IV injection of 100 micrograms CRH elicited significant decreases in LH concentrations during late follicular (-50%) and midluteal (-52%) phases of the cycle. LH concentrations decreased during the four-hours following injection of CRH and returned to those observed during the control period five hours after injection. Similarly, CRH elicited a significant decrease in FSH secretion during the midluteal phase of the cycle. CRH injection induced an increase in cortisol release during all phases of the cycle. These data demonstrate that exogenous CRH administration results in inhibition of gonadotropin secretion in late follicular and midluteal phases of the cycle. These results suggest that elevated endogenous CRH levels resulting in increased cortisol secretion could contribute to decreased gonadotropin secretion and, thus, disruption of reproductive function during stressful conditions in women.
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PMID:Corticotropin-releasing hormone inhibition of gonadotropin secretion during the menstrual cycle. 249 12

The application of immunogold techniques to localize pituitary hormones produces label that can be quantified and correlated with different secretory states. This report focuses on three major applications of the technology. In the first set of studies, immunogold labels for adrenocorticotropin (ACTH) or luteinizing hormone (LH beta) and follicle-stimulating hormone (FSH beta) were applied to ultrathin sections of pituitaries from adrenalectomized rats or from rats in different stages of the estrous cycle. During the first week after adrenalectomy, ACTH cell area increased. The concentration of immunoperoxidase label (amount of label/area of the corticotropes) decreased. Counts of gold markers showed that there were no changes in the concentration of antigens per granule. Three weeks after adrenalectomy, the amount of immunoperoxidase label increased along with the concentration of that label. The concentration of gold label for ACTH on granules also increased. All changes correlated well with increases in serum ACTH stimulated by adrenalectomy. In the studies of cycling rats, gonadotropes showed increases in the number of gold markers for LH beta or FSH beta per granule area just before an elevation in serum levels. There were also increases in the proportion of granules that contained only LH beta or FSH beta (monohormonal) before the rise in secretion. Thus, nonparallel release of gonadotropins might be attributed to changes in the ratio of gonadotropins packaged per granule. In the second series of studies, avidin-gold labels were used to identify sites of binding of biotinylated ligands. These studies illustrate and quantify binding by biotinylated gonadotropin-releasing hormone (GnRH) to ovarian or pituitary target cells. Triple-labeling protocols (avidin-peroxidase followed by immunogold) show that the target cells in the pituitary contain gonadotropins. In the third set of studies, avidin gold or avidin peroxidase was used to label sites of hybridization of a biotinylated cRNA probe to gonadotropin beta subunit mRNA. The sites of hybridization appear on rough endoplasmic reticulum; however, further work is needed to improve cell ultrastructure and perserve antigens. Triple-labeling protocols (avidin-peroxidase followed by immunogold) show the feasibility of the technique as well as the need for further refinement. To summarize, these studies describe multiple applications of gold labels for the localization of antigens, ligands, and mRNA. The labels are sensitive for detection of antigens and ligands and easily quantified. Quantitative analyses show changes in concentration of gold label that correlate well with secretory states.
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PMID:Localization and quantification of hormones, ligands, and mRNA with affinity-gold probes. 254 76

Experiments were conducted to test the hypothesis that acute TCDD toxicity is associated with pituitary hypofunction. Sexually mature male Sprague-Dawley rats were given graded doses of TCDD (0-100 micrograms/kg) and evaluated 7 days later. Despite pronounced hypophagia and body weight loss, plasma concentrations of growth hormone (GH), follicle-stimulating hormone (FSH), and luteinizing hormone (LH) were not significantly affected by any dose of TCDD. Only prolactin (PRL) concentrations were reduced, while, as previously reported, thyroid-stimulating hormone concentrations were elevated. Also, plasma LH, PRL, and adrenocorticotropic hormone (ACTH) concentrations were not significantly affected 1, 2, 3, 4, 5, or 7 days after a single dose of TCDD (50 micrograms/kg). We conclude that (1) pituitary hypofunction is not a major cause of the initial stages of acute TCDD toxicity, (2) growth retardation in TCDD-treated rats is not the result of a deficiency of GH, (3) alterations in plasma corticosterone concentrations are due to altered responsiveness of the adrenal to ACTH stimulation rather than to changes in plasma ACTH concentrations, and (4) that impaired spermatogenesis is not associated with a decrease in plasma FSH concentrations. In addition, the lack of a consistent effect on plasma PRL concentrations suggests that alterations in plasma PRL concentrations do not play a critical role in the toxicity of TCDD. Finally, because TCDD treatment causes a serious androgenic deficiency without increasing the rates at which androgens are catabolized or excreted, the fact that plasma LH concentrations were unaffected indicates that TCDD treatment must reduce the responsiveness of the testis to LH stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma concentrations of pituitary hormones in 2,3,7,8-tetrachlorodibenzo-p-dioxin-treated male rats. 255 21

The present study was undertaken in order to assess the influence of aging on the endogenous opioid control of gonadotropin and adrenocorticotropin/cortisol secretion in man. For this purpose, the capability of the opioid antagonist naloxone to increase circulating levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH) and cortisol was tested in male subjects of different ages. Thirty normal men were randomly chosen and divided into 3 groups by age: group I = 22-40 years (n = 10); group II = 41-59 years (n = 10); group III = 62-80 years (n = 10). Since the men of group III showed higher basal serum gonadotropin concentrations than the subjects of group I and group II, we selected from a large population a fourth group of elderly men with normal basal LH and FSH levels: group IV = 61-82 years (n = 7). All subjects were tested for 120 min during the intravenous administration of naloxone (4 mg given in an intravenous bolus at time 0, plus 10 mg infused for 2 h). Control tests with normal saline instead of naloxone were performed in all groups. All subjects had similar blood testosterone and cortisol levels, whereas LH and FSH concentrations were significantly higher in group III than in groups I, II and IV. Naloxone increased plasma cortisol concentrations by 50% in all groups. The cortisol secretory response followed a similar pattern regardless of age.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Different effects of aging on the opioid mechanisms controlling gonadotropin and cortisol secretion in man. 256 Apr 54

Immunoreactive (IR) prolactin was localized immunocytochemically in cell bodies in the mediobasal hypothalamus and in fibers in many regions of the rat brain. The cell bodies were found in the arcuate nuclei and the adjacent areas ventral to the ventromedial nuclei. Fiber projections extended rostrally to and/or through the anterior hypothalamus, preoptic area, nucleus accumbens, septum, diagonal bands of Broca, caudate-putamen, frontal cortex and accessory olfactory bulb; laterally to the amygdala, especially the central nucleus and some parts of the medial nucleus; caudally to and/or through the midbrain central gray, reticular formation, parabrachial region, and several portions of the lower brain stem and spinal cord extending to sacral levels. The system appears to be essentially identical to that containing proopiomelanocortin (POMC) and its processed peptides, as shown by double immunocytochemistry. Preabsorption of the antiprolactin antiserum with either prolactin or the 16,000-dalton N-terminus of POMC eliminated immunoreactivity in the brain. Preabsorption with other POMC-derived peptides, including beta-lipotropic hormone, beta-endorphin, met-enkephalin, adrenocorticotrophic hormone (1-24), corticotropin-like intermediate lobe peptide, alpha- and gamma-melanocyte-stimulating hormones and an octapeptide region of the N-terminus of POMC bearing some homology with prolactin, did not eliminate immunoreactivity in the brain. Similarly, preabsorption with growth hormone, luteinizing hormone, follicle-stimulating hormone, motilin or fetuin did not eliminate immunoreactivity in the brain. The antiprolactin antiserum also recognized all cells in the intermediate lobe and a subset of cells in the anterior lobe of the Snell dwarf mouse pituitary. This immunoreactivity was eliminated by preabsorption of the antiserum with prolactin or with the 16,000-dalton N-terminus of POMC. These results suggest that IR prolactin in the brain may be related to the N-terminus of POMC. Additional results based on one- and two-dimensional gel electrophoresis and immunoblotting indicate that the antiprolactin antiserum used in the majority of the immunocytochemical studies recognized a number of proteins.
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PMID:Distribution and partial characterization of immunoreactive prolactin in the rat brain. 271 51

Fourteen null cell adenomas of the pituitary gland were examined immunohistochemically with antisera against three general neuroendocrine markers and 22 hormones. All cases showed positive immunostaining for neuron-specific enolase, ten cases for synaptophysin, and six cases expressed chromogranin immunoreactivity. Hormone immunoreactivity was detected in a few cells in ten of the 14 cases studied and the number of hormones demonstrated in each case was one or two. Thyroid-stimulating hormone was detected in five of the 14 cases, gastrin in four, beta-endorphin in two, calcitonin gene related peptide in one, prolactin in one, and follicle-stimulating hormone in one.
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PMID:Null cell adenomas of the pituitary gland. An immunohistochemical study. 276 82

Cells isolated from 24 autopsied adult human pituitary glands by enzymatic dissociation and Percoll density gradient methods were maintained in culture for up to 10 months. Using rabbit antisera specific for individual pituitary hormones and immunoperoxidase staining, we found a large number of cultured pituitary cells to react positively to growth hormone, prolactin, adrenocorticotropin, follicle-stimulating hormone, luteinizing hormone, and thyrotropin immunoreactions. Electron microscopic examination of cultured pituitary cells demonstrated the occurrence of secretory granules in cytoplasm characteristic of in vivo human pituitary cells. The hormone secretion in culture by these pituitary cells was confirmed by the detection of prolactin, thyrotropin, and follicle-stimulating hormone in the culture medium by radioimmunoassay.
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PMID:Hormonal secretion by adult pituitary cells in culture. 282 29

An immunocytochemical study was performed by the indirect peroxidase method on the pituitary tumour of 37 patients with clinical and biological signs of silent adenoma. Antisera were used against human PRL, human GH, ACTH1-24, human ACTH17-39, alpha-melanocyte stimulating hormone (alpha-MSH), human beta-endorphin, alpha-subunit of hCG (hCG-alpha), and beta-subunits of human LH (LH-beta), human FSH (FSH-beta) and human TSH (TSH-beta). Immunostaining in at least 5% of the tumour cell population, with one or more antisera, was present in 13 cases; hCG-alpha immunostaining was the one most frequently observed. Combined immunostaining was found in 7 cases. Exclusive immunostaining was present in 6 cases: 4 with hCG-alpha, 1 with ACTH1-24 and 1 with TSH-beta. It is concluded that a significant number of silent pituitary adenomas show a certain secretory pattern of pituitary hormones or subunits of glycoprotein hormones as revealed by the immunocytochemistry.
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PMID:The immunocytochemical heterogeneity of silent pituitary adenomas. 284 Jul 93


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