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)

A human foreskin organ culture system has been developed to study the response of human skin to hormonal stimulation. Foreskins are maintained in culture on floating plastic supports which allows the epidermal surface to be exposed to air while the dermis is bathed in nutrient medium. Both black and white human foreskins can be maintained in organ culture for at least 1 wk with no change in the tissue structure or cell viability as determined by histochemical staining and by dopa reaction staining. Tyrosinase activity in both black and white human foreskin cultures decays markedly during the first 2 d of culture to a new steady state level which remains stable throughout the culture period. Both black and white foreskin cultures consistently demonstrate 2- to 10-fold increases in tyrosinase activity when treated with theophylline (1 mM). Approximately 90% of all skin cultures examined showed an increase in enzyme activity when treated with this phosphodiesterase inhibitor. Dibutyryl cAMP (0.1 mM) and [Nle4, D-phe7]-alpha MSH (10(-8) M), were also found to markedly stimulate tyrosinase activity in some skin cultures, whereas alpha-MSH and prostaglandin E1 produced only an inconsistent and small increase in the activity of the enzyme. Histamine (1 microM), vitamin D3 (1 microM), and retinoic acid (1 microM) failed to stimulate tyrosinase activity in either white or black foreskin cultures. This hormone-responsive organ culture system can be utilized to characterize the molecular processes responsible for the regulation of tyrosinase and pigmentation in human skin.
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PMID:Hormonal stimulation of tyrosinase activity in human foreskin organ cultures. 216 16

Proopiomelanocortin and its derivative peptides alpha MSH and beta-endorphin are produced by Leydig cells. beta-Endorphin or another testicular opiate is believed to suppress Sertoli cell hypertrophy. The goal of this study was to determine the effects of another proopiomelanocortin-derived peptide on Sertoli cells. The activities of both alpha MSH and des-acetyl alpha MSH have been compared, since this latter peptide has been identified in testicular extracts. Both alpha MSH and des-acetyl alpha MSH stimulated cAMP accumulation in the media of primary Sertoli cell cultures when incubated in the presence of a phosphodiesterase inhibitor, FSH or forskolin. Both peptides shifted the FSH dose-response curve to the left, making the cells more sensitive to this gonadotropin. The apparent potencies of alpha MSH and its des-acetyl derivative, as measured in Sertoli cells, were similar. We conclude that the MSHs are one of a group of modulators regulating Sertoli cells via the cAMP system, and Sertoli cells are equally responsive to alpha MSH and des-acetyl alpha MSH, unlike central nervous system and melanocytes which show differential responses to these peptides.
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PMID:Stimulation of adenosine 3',5'-monophosphate production in rat Sertoli cells by alpha-melanotropin-stimulating hormone (alpha MSH) and des-acetyl alpha MSH. 241 22

The present studies were undertaken to characterize further the influence of synthetic human beta-endorphin (0.5 mg/h) on insulin and glucagon responses to intravenous glucose in humans. Infusion of beta-endorphin in 10 normal volunteers caused a clear-cut inhibition of the overall insulin responses to a glucose pulse (0.33 g/kg iv) with values of glucose disappearance rates in the diabetic range [0.89 +/- 0.09 (P less than 0.01) vs. saline 1.82 +/- 0.15%/min]. Glucose-induced glucagon suppression was significantly lower during beta-endorphin, a fact that could have contributed to the reduced glucose utilization rates. The infusion of theophylline (150 mg + 350 mg/h) to increase the intracellular cAMP activity by inhibiting phosphodiesterase completely reversed the inhibitory effect of beta-endorphin on glucose-induced insulin secretion. As a consequence, glucose disappearance rates rose to 1.77 +/- 0.18%/min. Theophylline did not influence significantly the glucagon-releasing effect of beta-endorphin as well as the reduced glucagon suppression. An infusion of exogenous calcium (100 mg as iv bolus + 5 mg/min) to raise serum calcium in the hypercalcemic range (15 mg/dl) and lysine acetylsalicylate (72 mg/min) to block the synthesis of endogenous prostaglandin E did not interfere with the inhibiting effect of beta-endorphin on insulin secretion. These data confirm that beta-endorphin stimulates glucagon and inhibits basal and glucose-stimulated insulin secretion and suggest that the opioid influences the intraislet adenylate cyclase activity.
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PMID:Beta-endorphin and islet hormone release in humans: evidence for interference with cAMP. 255 Nov 76

The presence of Ca2+ in the incubation medium was required for stimulation of the release of the immunoreactive beta-endorphin-like peptide (IR-beta-EP) from the dispersed cells of the neurointermediate lobe of rat pituitary gland by adenosine 3',5'-monophosphate (cAMP) analogs, a phosphodiesterase inhibitor, L-isoproterenol, cholera toxin and forskolin. The basal release observed in the absence of the stimulants was also dependent on the addition of Ca2+. A calcium antagonist (verapamil) inhibited the effects of the stimulants. A calcium ionophore (A23187) enhanced the release of IR-beta-EP, but did not stimulate the formation of cAMP. These findings suggest that Ca2+ has the essential role in the release of beta-endorphin from the neurointermediate lobe of rat pituitary gland.
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PMID:Involvement of calcium in the release of immunoreactive beta-endorphin-like peptide from dispersed cells of the neurointermediate lobe of the rat pituitary gland. 258 72

Calmodulin (CaM) content in rabbit reticulocyte and the influence of opioid peptides on CaM activity in its membrane were studied by a highly sensitive assay of CaM activity based on the stimulation of Calcium-dependent phosphodiesterase activity. The CaM contents in reticulocytes were higher than those in normal erythrocytes, both in the cytosol fraction and in the membrane fraction. Among the opioid peptides, beta-endorphin (beta-EP) and dynorphin-A-(1-13) (dyn) had a significant inhibitory effect on CaM activity in reticulocyte membrane. The effect was not antagonized by naloxone or Mr. 2266, nor influenced by increase of Ca2+ concentration, but was reversed by the addition of exogenous CaM. This implies that the action of beta-EP and dyn on reticulocyte membranes probably involves an non-opioid mechanism, in which CaM may be an important key of linkage.
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PMID:Calmodulin content in rabbit reticulocyte and the influence of opioid peptides on calmodulin activity in its membrane. 289 62

The involvement of calmodulin in the secretion of beta-endorphin from the mouse anterior pituitary tumor cell line, AtT-20, was investigated. The calmodulin inhibitor W7 potentiated secretion produced by 8-BrcAMP, and induced a secretory response to arginine vasopressin, which did not elevate beta-endorphin levels when added alone. Release of hormone in response to CRF was not affected. Calmodulin phosphodiesterase inhibitor 8-MeOMeMIX produced a dose-dependent increase in 8-BrcAMP stimulation, suggesting that inhibition of cAMP degradation is the mechanism of enhancement of 8-BrcAMP-induced secretion in the presence of W7.
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PMID:Modulation of beta-endorphin secretion from mouse pituitary tumor cells by calmodulin inhibitor W7. 296 20

We examined the effect of angiotensin II, a calcium-mobilizing hormone on polyphosphoinositide metabolism in isolated rat adrenal glomerulosa cells. In cells preloaded with [32P]phosphate or with [3H]inositol, stimulation with angiotensin resulted in an approx. 40% reduction in the radioactivity of triphosphoinositide (PtdIns4,5P2) within 15 s. Only a slight increase in radioactivity was observed in the subsequent 30 min. Changes in labelling of diphosphoinositide (PtdIns4P) showed similar kinetics. Incorporation studies also showed a reduction in the pool size of [32P]PtdIns4P and [32P]PtdIns4,5P2 in response to angiotensin. Production of inositol phosphates in the absence or presence of lithium, a cation-inhibiting myo-inositol-1-phosphatase, was examined in cells preloaded with [3H]inositol. The results indicate that the production rate of inositol tris- and bisphosphate shows a manifold increase in the first seconds of stimulation and remains enhanced for at least several minutes. The present data suggest that the rate of resynthesis of polyphosphoinositides also increases shortly after the activation of PtdIns4,5P2 phosphodiesterase. Corticotropin, a hormone acting via cyclic AMP, neither affected polyphosphoinositide metabolism nor modified the action of angiotensin II.
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PMID:Polyphosphoinositide metabolism in adrenal glomerulosa cells. 298 37

Continuous treatment (1-3 weeks) with imipramine or adrenocorticotropin (ACTH) decreases the responsiveness of the norepinephrine-coupled cyclic nucleotide generating system in rat brain cerebral cortex. Experiments were undertaken to determine which component of the second messenger system is influenced by the hormone and antidepressant. Neither treatment modified the amount or function of extractable stimulatory guanine nucleotide binding protein or the activities of adenylate cyclase or phosphodiesterase. While both imipramine and ACTH treatment decreased the cyclic AMP response to norepinephrine, only imipramine administration influenced the response to isoproterenol. ACTH treatment was found to reduce the alpha adrenergic potentiation of isoproterenol- and 2-chloroadenosine-stimulated cyclic AMP production, as well as reduce the sensitivity of the norepinephrine response to prazosin. These findings indicate that imipramine and ACTH treatments decrease the responsiveness of the rat brain norepinephrine-stimulated cyclic AMP generating system through actions on the alpha and beta adrenergic receptor components. The results suggest that noradrenergic receptor activity may be under the control of adrenal and/or pituitary hormones.
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PMID:Effect of imipramine and adrenocorticotropin administration on the rat brain norepinephrine-coupled cyclic nucleotide generating system: alterations in alpha and beta adrenergic components. 299 1

The effect of adrenocorticotropic hormone (ACTH) on the intracellular concentration of cyclic nucleotides was studied in cultures of neurons from embryonic chick cerebral hemispheres. Incubation of neurons with ACTH(1-24) in the presence of phosphodiesterase inhibitor isobutylmethylxanthine resulted in a sustained increase in cyclic AMP while rise in cyclic GMP level was transient. The values obtained for half-maximal stimulation were 0.5 microM and 0.03 nM for cyclic AMP and cyclic GMP respectively. Concomitantly, ACTH(1-24) stimulated guanylate cyclase activity (half-maximal stimulation at 0.02 nM). These results suggest the existence of two distinct populations of ACTH receptors in neurons and provide the first evidence that cyclic GMP does mediate the action of ACTH in neurons.
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PMID:Regulation of cyclic AMP and cyclic GMP levels by adrenocorticotropic hormone in cultured neurons. 300 Mar 76

The role of the second messengers cAMP and Ca++ in the control of proopiomelanocortin (POMC) gene expression was investigated with the use of hybridization with cloned complementary DNA probes. The effects of cAMP-related drugs on POMC messenger RNA (mRNA) levels were assessed in primary cultures of intermediate (IL) and anterior rat pituitary cells maintained in serum-free medium. 8-Bromo-cAMP (1 mM), but not 8-bromo-cGMP (1 mM), induced a 2-fold increase in IL and anterior lobe cell after 2 days of treatment. A similar increase was obtained with the adenylate cyclase-activating drugs forskolin (1 microM) and cholera toxin (100 ng/ml) or the phosphodiesterase inhibitor RO 20-1724 (100 microM). At 48 h, all these treatments had increased beta-endorphin accumulation in the medium and transiently decreased the cellular beta-endorphin content in IL cells, suggesting a parallel effect of cAMP-related drugs on secretion and biosynthesis. Incubating the cells with the Ca++ channel antagonists D600 (50 microM), verapamil (50 microM), and the dihydropyridine nifedipine (0.1 microM) decreased basal POMC mRNA levels, whereas the dihydropyridine BAYK 8644 (0.1 microM), which activates the Ca++ channel, increased POMC mRNA levels after 2 days. In addition, nifedipine decreased the stimulatory effect of forskolin, whereas BAYK 8644 further stimulated the forskolin-increased POMC mRNA levels in IL cells. We conclude that both Ca++ and cAMP may regulate the gene expression of POMC.
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PMID:Calcium ion and cyclic adenosine 3',5'-monophosphate regulate proopiomelanocortin messenger ribonucleic acid levels in rat intermediate and anterior pituitary lobes. 302 21


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